rspНаучно-практическая ревматологияRheumatology Science and Practice1995-44841995-4492IMA-PRESS, LLC10.14412/1995-4484-2019-452-461rsp-2759Research ArticleПРОГРЕСС В РЕВМАТОЛОГИИ В XXI ВЕКЕPROGRESS IN RHEUMATOLOGY IN THE XXI CENTURYИммуновоспалительные ревматические заболевания, связанные с интерфероном типа I: новые данныеIMMUNOINFLAMMATORY RHEUMATIC DISEASES ASSOCIATED WITH TYPE I INTERFERON: NEW EVIDENCEНасоновЕ. Л.NasonovE. L.

научный руководитель ФГБНУ «НИИР им. В.А. Насоновой», академик РАН, профессор, докт. мед. наук

115522, Москва, Каширское шоссе, 34А119991, Москва, ул. Трубецкая, 8, стр. 2

34A, Kashirskoe Shosse, Moscow 115522

8, Trubetskaya St., Build. 2, Moscow 119991

АвдееваА. С.AvdeevaA. S.

научный сотрудник лаборатории стандартизации терапии ревматических заболеваний, канд. мед. наук

115522, Москва, Каширское шоссе, 34А

34A, Kashirskoe Shosse, Moscow 115522

9056249400@mail.ruФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой», ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет)РоссияV.A. Nasonova Research Institute of Rheumatology; I.M. Sechenov First Moscow State Medical University (Sechenov University)Russian FederationФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой»РоссияV.A. Nasonova Research Institute of RheumatologyRussian Federation201916092019574452461Copyright © Насонов Е.Л., Авдеева А.С., 20192019Насонов Е.Л., Авдеева А.С.Nasonov E.L., Avdeeva A.S.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://rsp.mediar-press.net/rsp/article/view/2759

Иммуновоспалительные ревматические заболевания (ИВРЗ) – большая группа патологических состояний, в основе которых лежит нарушение иммунологической толерантности к собственным тканям, ведущее к воспалению и необратимым органным повреждениям. В обзоре рассмотрены современные представления о роли интерферонов типа I в иммунопатогенезе ИВРЗ, в первую очередь системной красной волчанки, и новые возможности персонифицированной терапии.

Immunoinflammatory rheumatic diseases (IIRDs) are a large group of pathological conditions with impaired immunological tolerance to autogenous tissues, leading to inflammation and irreversible organ damage. The review discusses current ideas on the role of type I interferons in the immunopathogenesis of IIRDs, primarily systemic lupus erythematosus, and new possibilities for personalized therapy.

иммуновоспалительные ревматические заболеванияинтерфероны типа Iинтерфероновый «автограф»системная красная волчанкаimmunoinflammatory rheumatic diseasestype I interferonsinterferon signaturesystemic lupus erythematosus.ReferencesНасонов ЕЛ, Александрова ЕН, Новиков АА. Аутоиммунные ревматические заболевания – проблемы иммунопатологии и персонифицированной терапии. Вестник Российской академии медицинских наук. 2015;70(2):169-82Nasonov EL, Aleksandrova EN, Novikov AA. Autoimmune rheumatic diseases – problems of immunopathology and personalized therapy. Vestnik Rossiiskoi Akademii Meditsinskikh Nauk. 2015;70(2):169-82 (In Russ.).Wang L, Wang F-S, Gershwin ME. Human autoimmune diseases: a comprehensive update. J Intern Med. 2015;278:369-95. doi: 10.1111/joim.12395Wang L, Wang F-S, Gershwin ME. Human autoimmune diseases: a comprehensive update. J Intern Med. 2015;278:369-95. doi: 10.1111/joim.12395Rö nnblom L, Eloranta M-L. The interferon signature in autoimmune diseases. Curr Opin Rheumatol. 2013;25:248-53. doi: 10.1097/BOR.0b013e32835c7e32Rö nnblom L, Eloranta M-L. The interferon signature in autoimmune diseases. Curr Opin Rheumatol. 2013;25:248-53. doi: 10.1097/BOR.0b013e32835c7e32Kretschmer S, Lee-Kirsch MA. Type I interferon-mediated autoinflammation and autoimmunity. Curr Opin Immunol. 2017;49:96-102. doi: 10.1016/j.coi.2017.09.003Kretschmer S, Lee-Kirsch MA. Type I interferon-mediated autoinflammation and autoimmunity. Curr Opin Immunol. 2017;49:96-102. doi: 10.1016/j.coi.2017.09.003Green DS, Young HA, Valencia JC. Current prospects of type II interferon γ signaling and autoimmunity. J Biol Chem. 2017;25;292(34):13925-33. doi: 10.1074/jbc.R116.774745Green DS, Young HA, Valencia JC. Current prospects of type II interferon γ signaling and autoimmunity. J Biol Chem. 2017;25;292(34):13925-33. doi: 10.1074/jbc.R116.774745Psarras A, Emery P, Vital EM. Type I interferon-mediated autoimmune diseases: pathogenesis, diagnosis and targeted therapy. Rheumatology (Oxford). 2017;56(10):1662-75. doi: 10.1093/rheumatology/kew431Psarras A, Emery P, Vital EM. Type I interferon-mediated autoimmune diseases: pathogenesis, diagnosis and targeted therapy. Rheumatology (Oxford). 2017;56(10):1662-75. doi: 10.1093/rheumatology/kew431Muskardin TLW, Niewold TB. Type I interferon in rheumatic diseases. Nat Rev Rheumatol. 2018;14(4):214-28. doi: 10.1038/nrrheum.2018.31Muskardin TLW, Niewold TB. Type I interferon in rheumatic diseases. Nat Rev Rheumatol. 2018;14(4):214-28. doi: 10.1038/nrrheum.2018.31Schneider WM, Chevillotte MD, Rice CM. Interferon-stimulated genes: a complex web of host defenses. Annu Rev Immunol. 2014;32:513-45. doi: 10.1146/annurev-immunol-032713-120231Schneider WM, Chevillotte MD, Rice CM. Interferon-stimulated genes: a complex web of host defenses. Annu Rev Immunol. 2014;32:513-45. doi: 10.1146/annurev-immunol-032713-120231Banchereau R, Cepika AM, Banchereau J, Pascual V. Understanding Human Autoimmunity and Autoinflammation Through Transcriptomics. Annu Rev Immunol. 2017;35:337-70. doi: 10.1146/annurev-immunol-051116-052225Banchereau R, Cepika AM, Banchereau J, Pascual V. Understanding Human Autoimmunity and Autoinflammation Through Transcriptomics. Annu Rev Immunol. 2017;35:337-70. doi: 10.1146/annurev-immunol-051116-052225Ivashkiv LB, Donlin LT. Regulation of type I interferon responses. Nat Rev Immunol. 2014;14:36-49. doi: 10.1038/nri3581Ivashkiv LB, Donlin LT. Regulation of type I interferon responses. Nat Rev Immunol. 2014;14:36-49. doi: 10.1038/nri3581Crow YJ. Type I interferonopathies: a novel set of inborn errors of immunity: type I interferonopathies. Ann N Y Acad Sci Nov. 2011;1238:91-8. doi: 10.1111/j.1749-6632.2011.06220.xIvashkiv LB, Donlin LT. Regulation of type I interferon responses. Nat Rev Immunol. 2014;14:36-49. doi: 10.1038/nri3581Ioannou Y, Isenberg DA. Current evidence for the induction of autoimmune rheumatic manifestations by cytokine therapy. Arthritis Rheum. 2000;43:1431-42. doi: 10.1002/1529-0131(200007)43:7<1431::AID-ANR3>3.0.CO;2-ECrow YJ. Type I interferonopathies: a novel set of inborn errors of immunity: type I interferonopathies. Ann N Y Acad Sci Nov. 2011;1238:91-8. doi: 10.1111/j.1749-6632.2011.06220.xPicard C, Belot A. Does type-I interferon drive systemic autoimmunity? Autoimmun Rev. 2017;16(9):897-902. doi: 10.1016/j.autrev.2017.07.001Crow YJ. Type I interferonopathies: a novel set of inborn errors of immunity: type I interferonopathies. Ann N Y Acad Sci Nov. 2011;1238:91-8. doi: 10.1111/j.1749-6632.2011.06220.xHiggs BW, Liu Z, White B, et al. Patients with systemic lupus erythematosus, myositis, rheumatoid arthritis and scleroderma share activation of a common type I interferon pathway. Ann Rheum Dis. 2011;70:2029-36. doi: 10.1136/ard.2011.150326Ioannou Y, Isenberg DA. Current evidence for the induction of autoimmune rheumatic manifestations by cytokine therapy. Arthritis Rheum. 2000;43:1431-42. doi: 10.1002/1529-0131(200007)43:7<1431::AID-ANR3>3.0.CO;2-EChasset F, Arnaud L. Targeting interferons and their pathways in systemic lupus erythematosus. Autoimmun Rev. 2018;17:44-52. doi: 10.1016/j.autrev.2017.11.009Ioannou Y, Isenberg DA. Current evidence for the induction of autoimmune rheumatic manifestations by cytokine therapy. Arthritis Rheum. 2000;43:1431-42. doi: 10.1002/1529-0131(200007)43:7<1431::AID-ANR3>3.0.CO;2-ECrow MK, Olferiev M, Kirou KA. Type I Interferons in Autoimmune Disease. Annu Rev Pathol. 2019;14:369-93. doi: 10.1146/annurev-pathol-020117-043952Picard C, Belot A. Does type-I interferon drive systemic autoimmunity? Autoimmun Rev. 2017;16(9):897-902. doi: 10.1016/j.autrev.2017.07.001Garcia-Romo GS, Caielli S, Vega B, et al. Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus. Sci Transl Med. 2011;3:ra20. doi: 10.1126/scitranslmed.3001201Picard C, Belot A. Does type-I interferon drive systemic autoimmunity? Autoimmun Rev. 2017;16(9):897-902. doi: 10.1016/j.autrev.2017.07.001Doedens JR, Jones WD, Hill K, et al. Blood-borne Rna correlates with disease activity and Ifn-stimulated gene expression in systemic lupus erythematosus. J Immunol. 2016;197:2854-63. doi: 10.4049/jimmunol.1601142Higgs BW, Liu Z, White B, et al. Patients with systemic lupus erythematosus, myositis, rheumatoid arthritis and scleroderma share activation of a common type I interferon pathway. Ann Rheum Dis. 2011;70:2029-36. doi: 10.1136/ard.2011.150326Mavragani CP, Sagalovskiy I, Guo Q, et al. Expression of long interspersed nuclear element 1 retroelements and induction of type I interferon in patients with systemic autoimmune disease. Arthritis Rheum. 2016;68:2686-96. doi: 10.1002/art.39795Higgs BW, Liu Z, White B, et al. Patients with systemic lupus erythematosus, myositis, rheumatoid arthritis and scleroderma share activation of a common type I interferon pathway. Ann Rheum Dis. 2011;70:2029-36. doi: 10.1136/ard.2011.150326Lee JY, Park JK, Lee EY, et al. Circulating exosomes from patients with systemic lupus erythematosus induce an proinflammatory immune response. Arthritis Res Ther. 2016;18:264. doi: 10.1186/s13075-016-1159-yChasset F, Arnaud L. Targeting interferons and their pathways in systemic lupus erythematosus. Autoimmun Rev. 2018;17:44-52. doi: 10.1016/j.autrev.2017.11.009Bengtsson AA, Rö nnblom L. Role of interferons in SLE. Best Pract Res Clin Rheumatol. 2017;31(3):415-28. doi: 10.1016/j.berh.2017.10.0Chasset F, Arnaud L. Targeting interferons and their pathways in systemic lupus erythematosus. Autoimmun Rev. 2018;17:44-52. doi: 10.1016/j.autrev.2017.11.009Eloranta ML, Rö nnblom L. Cause and consequences of the activated type I interferon system in SLE. J Mol Med (Berl). 2016;94(10):1103-10. doi: 10.1007/s00109-016-1421-4Crow MK, Olferiev M, Kirou KA. Type I Interferons in Autoimmune Disease. Annu Rev Pathol. 2019;14:369-93. doi: 10.1146/annurev-pathol-020117-043952Weckerle CE, Franek BS, Kelly JA, et al. Network analysis of associations between serum interferon-α activity, autoantibodies, and clinical features in systemic lupus erythematosus. Arthritis Rheum. 2011;63(4):1044-53. doi: 10.1002/art.30187Crow MK, Olferiev M, Kirou KA. Type I Interferons in Autoimmune Disease. Annu Rev Pathol. 2019;14:369-93. doi: 10.1146/annurev-pathol-020117-043952Baechler EC, Batliwalla FM, Karypis G, et al. Interferoninducible gene expression signature in peripheral blood cells of patients with severe lupus. Proc Natl Acad Sci U S A. 2003;100(5):2610-5. doi: 10.1073/pnas.0337679100Garcia-Romo GS, Caielli S, Vega B, et al. Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus. Sci Transl Med. 2011;3:ra20. doi: 10.1126/scitranslmed.3001201Munroe ME, Lu R, Zhao YD, et al. Altered type II interferon precedes autoantibody accrual and elevated type I interferon activity prior to systemic lupus erythematosus classification. Ann Rheum Dis. 2016;75(11):2014-21. doi: 10.1136/annrheumdis-2015-2081Garcia-Romo GS, Caielli S, Vega B, et al. Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus. Sci Transl Med. 2011;3:ra20. doi: 10.1126/scitranslmed.3001201Niewold TB, Hua J, Lehman TJ, et al. High serum IFN-α activity is a heritable risk factor for systemic lupus erythematosus. Genes Immun. 2007;8:492-502. doi: 10.1038/sj.gene.6364408Doedens JR, Jones WD, Hill K, et al. Blood-borne Rna correlates with disease activity and Ifn-stimulated gene expression in systemic lupus erythematosus. J Immunol. 2016;197:2854-63. doi: 10.4049/jimmunol.1601142Kariuki SN, Franek BS, Kumar AA, et al. Trait-stratified genome-wide association study identifies novel and diverse genetic associations with serologic and cytokine phenotypes in systemic lupus erythematosus. Arthritis Res Ther. 2010;12(4):R151. doi: 10.1186/ar3101Doedens JR, Jones WD, Hill K, et al. Blood-borne Rna correlates with disease activity and Ifn-stimulated gene expression in systemic lupus erythematosus. J Immunol. 2016;197:2854-63. doi: 10.4049/jimmunol.1601142Md Yusof MY, Psarras A, El-Sherbiny YM, et al. Prediction of autoimmune connective tissue disease in an at-risk cohort: prognostic value of a novel two-score system for interferon status. Ann Rheum Dis. 2018;77:1432-9. doi: 10.1136/annrheumdis-2018-213386Mavragani CP, Sagalovskiy I, Guo Q, et al. Expression of long interspersed nuclear element 1 retroelements and induction of type I interferon in patients with systemic autoimmune disease. Arthritis Rheum. 2016;68:2686-96. doi: 10.1002/art.39795Morimoto AM, Flesher DT, Yang J, et al. Association of endogenous anti-interferon-α autoantibodies with decreased interferonpathway and disease activity in patients with systemic lupus erythematosus. Arthritis Rheum. 2011;63:2407-15. doi: 10.1002/art.30399Mavragani CP, Sagalovskiy I, Guo Q, et al. Expression of long interspersed nuclear element 1 retroelements and induction of type I interferon in patients with systemic autoimmune disease. Arthritis Rheum. 2016;68:2686-96. doi: 10.1002/art.39795Landolt-Marticorena C, Bonventi G, Lubovich A, et al. Lack of association between the interferon-alpha signature and longitudinal changes in disease activity in systemic lupus erythematosus. Ann Rheum Dis. 2009;68(9):1440-6. doi: 10.1136/ard.2008.093146Lee JY, Park JK, Lee EY, et al. Circulating exosomes from patients with systemic lupus erythematosus induce an proinflammatory immune response. Arthritis Res Ther. 2016;18:264. doi: 10.1186/s13075-016-1159-yPetri M, Singh S, Tesfasyone H, et al. Longitudinal expression of type I interferon responsive genes in systemic lupus erythematosus. Lupus. 2009;18(11):980-9. doi: 10.1177/0961203309105529Lee JY, Park JK, Lee EY, et al. Circulating exosomes from patients with systemic lupus erythematosus induce an proinflammatory immune response. Arthritis Res Ther. 2016;18:264. doi: 10.1186/s13075-016-1159-yRose T, Grutzkau A, Klotsche J, et al. Are interferon-related biomarkers advantageous for monitoring disease activity in systemic lupus erythematosus? A longitudinal benchmark study. Rheumatology (Oxford). 2017;56:1618-26. doi: 10.1093/rheumatology/kex220Bengtsson AA, Rö nnblom L. Role of interferons in SLE. Best Pract Res Clin Rheumatol. 2017;31(3):415-28. doi: 10.1016/j.berh.2017.10.0Connelly KL, Kandane-Rathayake R, Huq M, et al. Longitudinal association of type 1 interferon-induced chemokines with disease activity in systemic lupus erythematosus. Scientific Report. 2018;8:3268. doi: 10.1038/s41598-018-20203-9Bengtsson AA, Rö nnblom L. Role of interferons in SLE. Best Pract Res Clin Rheumatol. 2017;31(3):415-28. doi: 10.1016/j.berh.2017.10.0Banchereau R, Hong S, Cantarel B, et al. Personalized Immunomonitoring Uncovers Molecular Networks that Stratify Lupus Patients. Cell. 2016;165(3):551-65. doi: 10.1016/j.cell.2016.03.008Eloranta ML, Rö nnblom L. Cause and consequences of the activated type I interferon system in SLE. J Mol Med (Berl). 2016;94(10):1103-10. doi: 10.1007/s00109-016-1421-4Ghodke-Puranik Y, Niewold TB. Genetics of the type I interferon pathway in systemic lupus erythematosus. Int J Clin Rheumtol. 2013;8:657-69. doi: 10.2217/ijr.13.58Eloranta ML, Rö nnblom L. Cause and consequences of the activated type I interferon system in SLE. J Mol Med (Berl). 2016;94(10):1103-10. doi: 10.1007/s00109-016-1421-4Langefeld CD, Ainsworth HC, Cunninghame Graham DS, et al. Transancestral mapping and genetic load in systemic lupus erythematosus. Nat Commun. 2017;8:16021. doi: 10.1038/ncomms16021Weckerle CE, Franek BS, Kelly JA, et al. Network analysis of associations between serum interferon-α activity, autoantibodies, and clinical features in systemic lupus erythematosus. Arthritis Rheum. 2011;63(4):1044-53. doi: 10.1002/art.30187Niewold TB, Kelly JA, Kariuki SN, et al. IRF5 haplotypes demonstrate diverse serological associations which predict serum interferon alpha activity and explain the majority of the genetic association with systemic lupus erythematosus. Ann Rheum Dis. 2012;71(3):463-8. doi: 10.1136/annrheumdis-2011-200463Weckerle CE, Franek BS, Kelly JA, et al. Network analysis of associations between serum interferon-α activity, autoantibodies, and clinical features in systemic lupus erythematosus. Arthritis Rheum. 2011;63(4):1044-53. doi: 10.1002/art.30187Hagberg N, Joelsson M, Leonard D, et al. The Stat4 Sle risk allele Rs7574865[T] is associated with increased Il-12-induced IFN-γ production in T cells from patients with SLE. Ann Rheum Dis. 2018;77(7):1070-7. doi: 10.1136/annrheumdis-2017-212794Baechler EC, Batliwalla FM, Karypis G, et al. Interferoninducible gene expression signature in peripheral blood cells of patients with severe lupus. Proc Natl Acad Sci U S A. 2003;100(5):2610-5. doi: 10.1073/pnas.0337679100Lessard CJ, Li H, Adrianto I, et al. Variants at multiple loci implicated in both innate and adaptive immune responses are associated with Sjö gren's syndrome. Nat Genet. 2013;45(11):1284-92. doi: 10.1038/ng.2792Baechler EC, Batliwalla FM, Karypis G, et al. Interferoninducible gene expression signature in peripheral blood cells of patients with severe lupus. Proc Natl Acad Sci U S A. 2003;100(5):2610-5. doi: 10.1073/pnas.0337679100Angiolilli C, Marut W, van der Kroef M, et al. New insights into the genetics and epigenetics of systemic sclerosis. Nat Rev Rheumatol. 2018;14(11):657-73. doi: 10.1038/s41584-018-0099-0Munroe ME, Lu R, Zhao YD, et al. Altered type II interferon precedes autoantibody accrual and elevated type I interferon activity prior to systemic lupus erythematosus classification. Ann Rheum Dis. 2016;75(11):2014-21. doi: 10.1136/annrheumdis-2015-2081Dieguez-Gonzalez R, Calaza M, Perez-Pampin E, et al. Association of interferon regulatory factor 5 haplotypes, similar to that found in systemic lupus erythematosus, in a large subgroup of patients with rheumatoid arthritis. Arthritis Rheum. 2008;58:1264-74. doi: 10.1002/art.23426Munroe ME, Lu R, Zhao YD, et al. Altered type II interferon precedes autoantibody accrual and elevated type I interferon activity prior to systemic lupus erythematosus classification. Ann Rheum Dis. 2016;75(11):2014-21. doi: 10.1136/annrheumdis-2015-2081Nordang GB, Viken MK, Amundsen SS, et al. Interferon regulatory factor 5 gene polymorphism confers risk to several rheumatic diseases and correlates with expression of alternative thymic transcripts. Rheumatology (Oxford). 2012;51(4):619-26. doi: 10.1093/rheumatology/ker364Niewold TB, Hua J, Lehman TJ, et al. High serum IFN-α activity is a heritable risk factor for systemic lupus erythematosus. Genes Immun. 2007;8:492-502. doi: 10.1038/sj.gene.6364408Demirkaya E, Zhou Q, Smith CK, et al. Brief report: deficiency of complement 1r subcomponent in early-onset systemic lupus erythematosus: the role of disease-modifying alleles in a monogenic disease. Arthritis Rheum. 2017;69:1832-9. doi: 10.1002/art.40158Niewold TB, Hua J, Lehman TJ, et al. High serum IFN-α activity is a heritable risk factor for systemic lupus erythematosus. Genes Immun. 2007;8:492-502. doi: 10.1038/sj.gene.6364408Ghodke-Puranik Y, Dorschner JM, Vsetecka DM, et al. Lupusassociated functional polymorphism in Pnp causes cell cycle abnormalities and interferon pathway activation in human immune cells. Arthritis Rheum. 2017;69:2328-37. doi: 10.1002/art.40304Kariuki SN, Franek BS, Kumar AA, et al. Trait-stratified genome-wide association study identifies novel and diverse genetic associations with serologic and cytokine phenotypes in systemic lupus erythematosus. Arthritis Res Ther. 2010;12(4):R151. doi: 10.1186/ar3101Kariuki SN, Ghodke-Puranik Y, Dorschner JM, et al. Genetic analysis of the pathogenic molecular sub-phenotype interferonalpha identifies multiple novel loci involved in systemic lupus erythematosus. Genes Immun. 2015;16:15-23. doi: 10.1038/gene.2014.57Kariuki SN, Franek BS, Kumar AA, et al. Trait-stratified genome-wide association study identifies novel and diverse genetic associations with serologic and cytokine phenotypes in systemic lupus erythematosus. Arthritis Res Ther. 2010;12(4):R151. doi: 10.1186/ar3101Faridi MH, Khan SQ, Zhao W, et al. Cd11b activation suppresses TLR-dependent inflammation and autoimmunity in systemic lupus erythematosus. J Clin Invest. 2017;127:1271-83. doi: 10.1172/JCI88442Md Yusof MY, Psarras A, El-Sherbiny YM, et al. Prediction of autoimmune connective tissue disease in an at-risk cohort: prognostic value of a novel two-score system for interferon status. Ann Rheum Dis. 2018;77:1432-9. doi: 10.1136/annrheumdis-2018-213386Coit P, Jeffries M, Altorok N, et al. Genome-wide DNA methylation study suggests epigenetic accessibility and transcriptional poising of interferon-regulated genes in naive CD4+ T cells from lupus patients. J Autoimmun. 2013;43:78-84.Md Yusof MY, Psarras A, El-Sherbiny YM, et al. Prediction of autoimmune connective tissue disease in an at-risk cohort: prognostic value of a novel two-score system for interferon status. Ann Rheum Dis. 2018;77:1432-9. doi: 10.1136/annrheumdis-2018-213386doi: 10.1016/j.jaut.2013.04.003Morimoto AM, Flesher DT, Yang J, et al. Association of endogenous anti-interferon-α autoantibodies with decreased interferonpathway and disease activity in patients with systemic lupus erythematosus. Arthritis Rheum. 2011;63:2407-15. doi: 10.1002/art.30399Cheng J, Wu R, Long L, et al. Mirna-451a targets Ifn regulatory factor 8 for the progression of systemic lupus erythematosus. Inflammation. 2017;40:676-87. doi: 10.1007/s10753-017-0514-8Morimoto AM, Flesher DT, Yang J, et al. Association of endogenous anti-interferon-α autoantibodies with decreased interferonpathway and disease activity in patients with systemic lupus erythematosus. Arthritis Rheum. 2011;63:2407-15. doi: 10.1002/art.30399Smith S, Fernando T, Wu PW, et al. Microrna-302d targets Irf9 to regulate the Ifn-induced gene expression in SLE. J Autoimmun. 2017;79:105-11. doi: 10.1016/j.jaut.2017.03.003Landolt-Marticorena C, Bonventi G, Lubovich A, et al. Lack of association between the interferon-alpha signature and longitudinal changes in disease activity in systemic lupus erythematosus. Ann Rheum Dis. 2009;68(9):1440-6. doi: 10.1136/ard.2008.093146Van den Hoogen LL, van Roon JAG, Mertens JS, et al. Galectin-9 is an easy to measure biomarker for the interferon signature in systemic lupus erythematosus and antiphospholipid syndrome. Ann Rheum Dis. 2018;77(12):1810-4. doi: 10.1136/annrheumdis-2018-213497Landolt-Marticorena C, Bonventi G, Lubovich A, et al. Lack of association between the interferon-alpha signature and longitudinal changes in disease activity in systemic lupus erythematosus. Ann Rheum Dis. 2009;68(9):1440-6. doi: 10.1136/ard.2008.093146Oliveira JJ, Karrar S, Rainbow DB, et al. The plasma biomarker soluble SIGLEC-1 is associated with the type I interferon transcriptional signature, ethnic background and renal disease in systemic lupus erythematosus. Arthritis Res Ther. 2018;20(1):152. doi: 10.1186/s13075-018-1649-1Petri M, Singh S, Tesfasyone H, et al. Longitudinal expression of type I interferon responsive genes in systemic lupus erythematosus. Lupus. 2009;18(11):980-9. doi: 10.1177/0961203309105529Lü bbers J, Brink M, van de Stadt LA, et al. The type I IFN signature as a biomarker of preclinical rheumatoid arthritis. Ann Rheum Dis. 2013;72(5):776-80. doi: 10.1136/annrheumdis-2012-2Petri M, Singh S, Tesfasyone H, et al. Longitudinal expression of type I interferon responsive genes in systemic lupus erythematosus. Lupus. 2009;18(11):980-9. doi: 10.1177/0961203309105529Thurlings RM, Boumans M, Tekstra J, et al. Relationship between the type I interferon signature and the response to rituximab in rheumatoid arthritis patients. Arthritis Rheum. 2010;62:3607-14. doi: 10.1002/art.27702Rose T, Grutzkau A, Klotsche J, et al. Are interferon-related biomarkers advantageous for monitoring disease activity in systemic lupus erythematosus? A longitudinal benchmark study. Rheumatology (Oxford). 2017;56:1618-26. doi: 10.1093/rheumatology/kex220Raterman HG, Vosslamber S, De RS, et al. The interferon type I signature towards prediction of non-response to rituximab in rheumatoid arthritis patients. Arthritis Res Ther. 2012;14:R95. doi: 10.1186/ar3819Rose T, Grutzkau A, Klotsche J, et al. Are interferon-related biomarkers advantageous for monitoring disease activity in systemic lupus erythematosus? A longitudinal benchmark study. Rheumatology (Oxford). 2017;56:1618-26. doi: 10.1093/rheumatology/kex220Sanayama Y, Ikeda K, Saito Y, et al. Prediction of therapeutic responses to tocilizumab in patients with rheumatoid arthritis: biomarkers identified by analysis of gene expression in peripheral blood mononuclear cells using genome-wide DNA microarray. Arthritis Rheum. 2014;66(6):1421-31. doi: 10.1002/art.38400Connelly KL, Kandane-Rathayake R, Huq M, et al. Longitudinal association of type 1 interferon-induced chemokines with disease activity in systemic lupus erythematosus. Scientific Report. 2018;8:3268. doi: 10.1038/s41598-018-20203-9Mavragani CP, La DT, Stohl W, Crow MK. Association of the response to tumor necrosis factor antagonists with plasma type I interferon activity and interferon-β/α ratios in rheumatoid arthritis patients: a post hoc analysis of a predominantly Hispanic cohort. Arthritis Rheum. 2010;62:392-401. doi: 10.1002/art.27226Connelly KL, Kandane-Rathayake R, Huq M, et al. Longitudinal association of type 1 interferon-induced chemokines with disease activity in systemic lupus erythematosus. Scientific Report. 2018;8:3268. doi: 10.1038/s41598-018-20203-9Wampler Muskardin T, Vashisht P, Dorschner JM, et al. Increased pretreatment serum IFN-β/α ratio predicts non-response to tumour necrosis factor α inhibition in rheumatoid arthritis. Ann Rheum Dis. 2016;75(10):1757-62. doi: 10.1136/annrheumdis-2015-208001Banchereau R, Hong S, Cantarel B, et al. Personalized Immunomonitoring Uncovers Molecular Networks that Stratify Lupus Patients. Cell. 2016;165(3):551-65. doi: 10.1016/j.cell.2016.03.008De Jong TD, Blits M, de Ridder S, et al. Type I interferon response gene expression in established rheumatoid arthritis is not associated with clinical parameters. Arthritis Res Ther. 2016;18:Article number 290. doi: 10.1186/s13075-016-1191-yBanchereau R, Hong S, Cantarel B, et al. Personalized Immunomonitoring Uncovers Molecular Networks that Stratify Lupus Patients. Cell. 2016;165(3):551-65. doi: 10.1016/j.cell.2016.03.008De Jong TD, Vosslamber S, Blits M, et al. Effect of prednisone on type I interferon signature in rheumatoid arthritis: consequences for response prediction to rituximab. Arthritis Res Ther. 2015;17:78. doi: 10.1186/s13075-015-0564-yGhodke-Puranik Y, Niewold TB. Genetics of the type I interferon pathway in systemic lupus erythematosus. Int J Clin Rheumtol. 2013;8:657-69. doi: 10.2217/ijr.13.58De Jong TD, Snoek T, Mantel E, et al. Dynamics of the Type I Interferon Response During Immunosuppressive Therapy in Rheumatoid Arthritis. Front Immunol. 2019 Apr 24;10:902. doi: 10.3389/fimmu.2019.00902Ghodke-Puranik Y, Niewold TB. Genetics of the type I interferon pathway in systemic lupus erythematosus. Int J Clin Rheumtol. 2013;8:657-69. doi: 10.2217/ijr.13.58Thorlacius GE, Wahren-Herlenius M, Ronnblom L. An update on the role of type I interferons in systemic lupus erythematosus and Sjogren's syndrome. Curr Opin Rheumatol. 2018;30:471-81. doi: 10.1097/BOR.0000000000000524Langefeld CD, Ainsworth HC, Cunninghame Graham DS, et al. Transancestral mapping and genetic load in systemic lupus erythematosus. Nat Commun. 2017;8:16021. doi: 10.1038/ncomms16021Nezos A, Gravani F, Tassidou A, et al. Type I and II interferon signatures in Sjogren's syndrome pathogenesis: contributions in distinct clinical phenotypes and Sjogren's related lymphomagenesis. J Autoimmun. 2015;63:47-58. doi: 10.1016/j.jaut.2015.07.002Langefeld CD, Ainsworth HC, Cunninghame Graham DS, et al. Transancestral mapping and genetic load in systemic lupus erythematosus. Nat Commun. 2017;8:16021. doi: 10.1038/ncomms16021Benchabane S, Belkhelfa M, Belguendouz H, et al. Interferon-γ inhibits inflammatory responses mediators via suppression of iNOS signaling pathway in PBMCs from patients with primary Sjö gren's syndrome. Inflammopharmacology. 2018;26:1165-74. doi: 10.1007/s10787-018-0499-4Niewold TB, Kelly JA, Kariuki SN, et al. IRF5 haplotypes demonstrate diverse serological associations which predict serum interferon alpha activity and explain the majority of the genetic association with systemic lupus erythematosus. Ann Rheum Dis. 2012;71(3):463-8. doi: 10.1136/annrheumdis-2011-200463Bodewes ILA, Al-Ali S, van Helden-Meeuwsen CG, et al. Systemic interferon type I and type II signatures in primary Sjö gren's syndrome reveal differences in biological disease activity. Rheumatology. 2018;57:921-30. doi: 10.1093/rheumatology/kex490Niewold TB, Kelly JA, Kariuki SN, et al. IRF5 haplotypes demonstrate diverse serological associations which predict serum interferon alpha activity and explain the majority of the genetic association with systemic lupus erythematosus. Ann Rheum Dis. 2012;71(3):463-8. doi: 10.1136/annrheumdis-2011-200463Dieude P, Guedj M, Wipff J, et al. STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. Arthritis Rheum. 2009;60:2472-9. doi: 10.1002/art.24688Hagberg N, Joelsson M, Leonard D, et al. The Stat4 Sle risk allele Rs7574865[T] is associated with increased Il-12-induced IFN-γ production in T cells from patients with SLE. Ann Rheum Dis. 2018;77(7):1070-7. doi: 10.1136/annrheumdis-2017-212794Gourh P, Agarwal SK, Divecha D, et al. Polymorphisms in TBX21 and STAT4 increase the risk of systemic sclerosis: evidence of possible gene-gene interaction and alterations in Th1/Th2 cytokines. Arthritis Rheum. 2009;60:3794-806. doi: 10.1002/art.24958Hagberg N, Joelsson M, Leonard D, et al. The Stat4 Sle risk allele Rs7574865[T] is associated with increased Il-12-induced IFN-γ production in T cells from patients with SLE. Ann Rheum Dis. 2018;77(7):1070-7. doi: 10.1136/annrheumdis-2017-212794Rueda B, Broen J, Simeon C, et al. The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype. Hum Mol Genet. 2009;18:2071-7. doi: 10.1093/hmg/ddp119Lessard CJ, Li H, Adrianto I, et al. Variants at multiple loci implicated in both innate and adaptive immune responses are associated with Sjö gren's syndrome. Nat Genet. 2013;45(11):1284-92. doi: 10.1038/ng.2792Skaug B, Assassi S. Type I interferon dysregulation in Systemic Sclerosis. Cytokine. 2019 Jan 23. doi: 10.1016/j.cyto.2018.12.018Lessard CJ, Li H, Adrianto I, et al. Variants at multiple loci implicated in both innate and adaptive immune responses are associated with Sjö gren's syndrome. Nat Genet. 2013;45(11):1284-92. doi: 10.1038/ng.2792Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis. Arthritis Rheum. 2014;66:714-25. doi: 10.1002/art.38288Angiolilli C, Marut W, van der Kroef M, et al. New insights into the genetics and epigenetics of systemic sclerosis. Nat Rev Rheumatol. 2018;14(11):657-73. doi: 10.1038/s41584-018-0099-0George PM, Oliver E, Dorfmuller P, et al. Evidence for the involvement of type I interferon in pulmonary arterial hypertension. Circ Res. 2014;114:677-88. doi: 10.1161/CIRCRESAHA.114.302221Angiolilli C, Marut W, van der Kroef M, et al. New insights into the genetics and epigenetics of systemic sclerosis. Nat Rev Rheumatol. 2018;14(11):657-73. doi: 10.1038/s41584-018-0099-0Brkic Z, van Bon L, Cossu M, et al. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis. Ann Rheum Dis. 2016;75(8):1567-73. doi: 10.1136/annrheumdis-2015-207Dieguez-Gonzalez R, Calaza M, Perez-Pampin E, et al. Association of interferon regulatory factor 5 haplotypes, similar to that found in systemic lupus erythematosus, in a large subgroup of patients with rheumatoid arthritis. Arthritis Rheum. 2008;58:1264-74. doi: 10.1002/art.23426Van den Hoogen LL, Fritsch-Stork RD, Versnel MA, et al. Monocyte type I interferon signature in antiphospholipid syndrome is related to proinflammatory monocyte subsets, hydroxychloroquine and statin use. Ann Rheum Dis. 2016;75:e81. doi: 10.1136/annrheumdis-2016-210485Dieguez-Gonzalez R, Calaza M, Perez-Pampin E, et al. Association of interferon regulatory factor 5 haplotypes, similar to that found in systemic lupus erythematosus, in a large subgroup of patients with rheumatoid arthritis. Arthritis Rheum. 2008;58:1264-74. doi: 10.1002/art.23426Ugolini-Lopes MR, Torrezan GT, Gandara APR, et al. Enhanced type I interferon gene signature in primary antiphospholipid syndrome: Association with earlier disease onset and preeclampsia. Autoimmun Rev. 2019;18(4):393-8. doi: 10.1016/j.autrev.2018.11.004Nordang GB, Viken MK, Amundsen SS, et al. Interferon regulatory factor 5 gene polymorphism confers risk to several rheumatic diseases and correlates with expression of alternative thymic transcripts. Rheumatology (Oxford). 2012;51(4):619-26. doi: 10.1093/rheumatology/ker364Palli E, Kravvariti E, Tektonidou MG. Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations. Front Immunol. 2019;10:487. doi: 10.3389/fimmu.2019.00487Nordang GB, Viken MK, Amundsen SS, et al. Interferon regulatory factor 5 gene polymorphism confers risk to several rheumatic diseases and correlates with expression of alternative thymic transcripts. Rheumatology (Oxford). 2012;51(4):619-26. doi: 10.1093/rheumatology/ker364Grenn RC, Yalavarthi S, Gandhi AA, et al. Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome. Ann Rheum Dis. 2017;76:450-7. doi: 10.1136/annrheumdis-2016-209442Demirkaya E, Zhou Q, Smith CK, et al. Brief report: deficiency of complement 1r subcomponent in early-onset systemic lupus erythematosus: the role of disease-modifying alleles in a monogenic disease. Arthritis Rheum. 2017;69:1832-9. doi: 10.1002/art.40158Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-β/α-mediated innate immune mechanisms in dermatomyositis. Ann Neurol. 2005;57:664-78. doi: 10.1002/ana.20464Demirkaya E, Zhou Q, Smith CK, et al. Brief report: deficiency of complement 1r subcomponent in early-onset systemic lupus erythematosus: the role of disease-modifying alleles in a monogenic disease. Arthritis Rheum. 2017;69:1832-9. doi: 10.1002/art.40158Liao AP, Salajegheh M, Nazareno R, et al. Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis. Ann Rheum Dis. 2011;70:831-6. doi: 10.1136/ard.2010.139949Ghodke-Puranik Y, Dorschner JM, Vsetecka DM, et al. Lupusassociated functional polymorphism in Pnp causes cell cycle abnormalities and interferon pathway activation in human immune cells. Arthritis Rheum. 2017;69:2328-37. doi: 10.1002/art.40304Somani A-K, Swick AR, Cooper KD, et al. Severe dermatomyositis triggered by interferon beta-1a therapy and associated with enhanced type I interferon signaling. Arch Dermatol. 2008;144:1341-9. doi: 10.1001/archderm.144.10.1341Ghodke-Puranik Y, Dorschner JM, Vsetecka DM, et al. Lupusassociated functional polymorphism in Pnp causes cell cycle abnormalities and interferon pathway activation in human immune cells. Arthritis Rheum. 2017;69:2328-37. doi: 10.1002/art.40304Piper CJM, Wilkinson MGL, Deakin CT, et al. CD19+CD24hiCD38hi B Cells Are Expanded in Juvenile Dermatomyositis and Exhibit a Pro-Inflammatory Phenotype After Activation Through Toll-Like Receptor 7 and Interferon-α. Front Immunol. 2018;9. doi: 10.3389/fimmu.2018.01372Kariuki SN, Ghodke-Puranik Y, Dorschner JM, et al. Genetic analysis of the pathogenic molecular sub-phenotype interferonalpha identifies multiple novel loci involved in systemic lupus erythematosus. Genes Immun. 2015;16:15-23. doi: 10.1038/gene.2014.57Oon S, Wilson NJ, Wicks I. Targeted therapeutics in SLE: emerging strategies to modulate the interferon pathway. Clin Transl Immunol. 2016;5:e79. doi: 10.1038/cti.2016.26Kariuki SN, Ghodke-Puranik Y, Dorschner JM, et al. Genetic analysis of the pathogenic molecular sub-phenotype interferonalpha identifies multiple novel loci involved in systemic lupus erythematosus. Genes Immun. 2015;16:15-23. doi: 10.1038/gene.2014.57Mathian A, Hie M, Cohen-Aubart F, et al. Targeting interferons in systemic lupus erythematosus: current and future prospects. Drugs. 2015;75:835-46. doi: 10.1007/s40265-015-0394-xFaridi MH, Khan SQ, Zhao W, et al. Cd11b activation suppresses TLR-dependent inflammation and autoimmunity in systemic lupus erythematosus. J Clin Invest. 2017;127:1271-83. doi: 10.1172/JCI88442Bodewes ILA, Gottenberg JE, van Helden-Meeuwsen CG, et al. Hydroxychloroquine treatment downregulates systemic interferon activation in primary Sjö gren's syndrome in the JOQUER randomized trial. Rheumatology (Oxford). 2019 Jun 25. doi: 10.1093/rheumatology/kez242Faridi MH, Khan SQ, Zhao W, et al. Cd11b activation suppresses TLR-dependent inflammation and autoimmunity in systemic lupus erythematosus. J Clin Invest. 2017;127:1271-83. doi: 10.1172/JCI88442Gardet A, Pellerin A, McCarl CA, et al. Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNγ Production From Patients Affected With Cutaneous Lupus Erythematosus. Front Immunol. 2019;10:275. doi: 10.3389/fimmu.2019.00275Coit P, Jeffries M, Altorok N, et al. Genome-wide DNA methylation study suggests epigenetic accessibility and transcriptional poising of interferon-regulated genes in naive CD4+ T cells from lupus patients. J Autoimmun. 2013;43:78-84. doi: 10.1016/j.jaut.2013.04.003Olsen NJ, McAloose C, Carter J, et al. Clinical and Immunologic Profiles in Incomplete Lupus Erythematosus and Improvement with Hydroxychloroquine Treatment. Autoimmune Dis. 2016:8791629. doi: 10.1155/2016/8791629Coit P, Jeffries M, Altorok N, et al. Genome-wide DNA methylation study suggests epigenetic accessibility and transcriptional poising of interferon-regulated genes in naive CD4+ T cells from lupus patients. J Autoimmun. 2013;43:78-84. doi: 10.1016/j.jaut.2013.04.003Eloranta ML, Lö vgren T, Finke D, et al. Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells. Arthritis Rheum. 2009;60:2418-27. doi: 10.1002/art.24686Cheng J, Wu R, Long L, et al. Mirna-451a targets Ifn regulatory factor 8 for the progression of systemic lupus erythematosus. Inflammation. 2017;40:676-87. doi: 10.1007/s10753-017-0514-8Berggren O, Hagberg N, Weber G, et al. B lymphocytes enhance the interferon-alpha production by plasmacytoid dendritic cells. Arthritis Rheum. 2012;64:3409-19. doi: 10.1002/art.34599Cheng J, Wu R, Long L, et al. Mirna-451a targets Ifn regulatory factor 8 for the progression of systemic lupus erythematosus. Inflammation. 2017;40:676-87. doi: 10.1007/s10753-017-0514-8Leonard D, Eloranta ML, Hagberg N, et al. Activated T cells enhance interferon-alpha production by plasmacytoid dendritic cells stimulated with RNA-containing immune complexes. Ann Rheum Dis. 2016;75(9):1728-34. doi: 10.1136/annrheumdis-2015-208055Smith S, Fernando T, Wu PW, et al. Microrna-302d targets Irf9 to regulate the Ifn-induced gene expression in SLE. J Autoimmun. 2017;79:105-11. doi: 10.1016/j.jaut.2017.03.003Skurkovich SV, Klinova EG, Eremkina EI, Levina NV. Immunosupressive effect of anti-interferon serum. Nature. 1974;247:551-2. doi: 10.1038/247551a0Smith S, Fernando T, Wu PW, et al. Microrna-302d targets Irf9 to regulate the Ifn-induced gene expression in SLE. J Autoimmun. 2017;79:105-11. doi: 10.1016/j.jaut.2017.03.003Skurkovich SV, Loukina GV, Sigidin YA, Skurkovich BS. Succesful first-time use of antibodies to interferon-gamma alone and combined with antibodies to tumor necrosis factor-alfa to treat rheumatic diseasers (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Behcet`s syndrome). Int J Immunother. 1998;14:23-32.Van den Hoogen LL, van Roon JAG, Mertens JS, et al. Galectin-9 is an easy to measure biomarker for the interferon signature in systemic lupus erythematosus and antiphospholipid syndrome. Ann Rheum Dis. 2018;77(12):1810-4. doi: 10.1136/annrheumdis-2018-213497Sigidin AY, Loukina GV, Skurkovich B, Skurkovich SV. Randomized double-blind trial of anti-interferob-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol. 2001;30:203-7. doi: 10.1080/030097401316909530Van den Hoogen LL, van Roon JAG, Mertens JS, et al. Galectin-9 is an easy to measure biomarker for the interferon signature in systemic lupus erythematosus and antiphospholipid syndrome. Ann Rheum Dis. 2018;77(12):1810-4. doi: 10.1136/annrheumdis-2018-213497Baker KF, Isaacs JD. Novel therapies for immune-mediated inflammatory diseases: What can we learn from their use in rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, psoriasis, Crohn's disease and ulcerative colitis? Ann Rheum Dis. 2018;77(2):175-87. doi: 10.1136/annrheumdis-2017-211555Oliveira JJ, Karrar S, Rainbow DB, et al. The plasma biomarker soluble SIGLEC-1 is associated with the type I interferon transcriptional signature, ethnic background and renal disease in systemic lupus erythematosus. Arthritis Res Ther. 2018;20(1):152. doi: 10.1186/s13075-018-1649-1Yao Y, Higgs BW, Morehouse C, et al. Development of potential pharmacodynamic and diagnostic markers for anti-IFN-alpha monoclonal antibody trials in systemic lupus erythematosus. Hum Genom Proteom. 2009:Article ID 374312. doi: 10.4061/2009/37431210.4061/2009/374312Oliveira JJ, Karrar S, Rainbow DB, et al. The plasma biomarker soluble SIGLEC-1 is associated with the type I interferon transcriptional signature, ethnic background and renal disease in systemic lupus erythematosus. Arthritis Res Ther. 2018;20(1):152. doi: 10.1186/s13075-018-1649-1Merrill JT, Wallace DJ, Petri M, et al. Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis. 2011;70:1905-13. doi: 10.1136/ard.2010.144485Lü bbers J, Brink M, van de Stadt LA, et al. The type I IFN signature as a biomarker of preclinical rheumatoid arthritis. Ann Rheum Dis. 2013;72(5):776-80. doi: 10.1136/annrheumdis-2012-2Petri M, Wallace DJ, Spindler A, et al. Sifalimumab, a human anti-interferon-alpha monoclonal antibody, in systemic lupus erythematosus: a phase I randomized, controlled, dose-escalation study. Arthritis Rheum. 2013;65:1011-21. doi: 10.1002/art.37824Lü bbers J, Brink M, van de Stadt LA, et al. The type I IFN signature as a biomarker of preclinical rheumatoid arthritis. Ann Rheum Dis. 2013;72(5):776-80. doi: 10.1136/annrheumdis-2012-2Khamashta M, Merrill JT, Werth VP, et al. Sifalimumab, an antiinterferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909-16. doi: 10.1136/annrheumdis-2015-208562Thurlings RM, Boumans M, Tekstra J, et al. Relationship between the type I interferon signature and the response to rituximab in rheumatoid arthritis patients. Arthritis Rheum. 2010;62:3607-14. doi: 10.1002/art.27702Tcherepanova I, Curtis M, Sale M, et al. SAT0193 Results of a randomized placebo controlled phase ia study of AGS-009, a humanized anti-interferon-α monoclonal antibody in subjects with systemic lupus erythematosus. Ann Rheum Dis. 2013;71(Suppl 3):536.3-7. doi: 10.1136/annrheumdis-2012-eular.3140Thurlings RM, Boumans M, Tekstra J, et al. Relationship between the type I interferon signature and the response to rituximab in rheumatoid arthritis patients. Arthritis Rheum. 2010;62:3607-14. doi: 10.1002/art.27702Kalunian KC, Merrill JT, Maciuca R, et al. A phase II study of the efficacy and safety of rontalizumab (rhuMAb interferon-α) in patients with systemic lupus erythematosus (ROSE). Ann Rheum Dis. 2016;75:196-202. doi: 10.1136/annrheumdis-2014-206090Raterman HG, Vosslamber S, De RS, et al. The interferon type I signature towards prediction of non-response to rituximab in rheumatoid arthritis patients. Arthritis Res Ther. 2012;14:R95. doi: 10.1186/ar3819Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7:428-39. doi: 10.1080/19420862.2015.1007810Raterman HG, Vosslamber S, De RS, et al. The interferon type I signature towards prediction of non-response to rituximab in rheumatoid arthritis patients. Arthritis Res Ther. 2012;14:R95. doi: 10.1186/ar3819Riggs JM, Hanna RN, Rajan B, et al. Characterisation of anifrolumab, a fully human anti-interferon receptor antagonist antibody for the treatment of systemic lupus erythematosus. Lupus Sci Med. 2018;5:e000261. doi: 10.1136/lupus-2018-000261Sanayama Y, Ikeda K, Saito Y, et al. Prediction of therapeutic responses to tocilizumab in patients with rheumatoid arthritis: biomarkers identified by analysis of gene expression in peripheral blood mononuclear cells using genome-wide DNA microarray. Arthritis Rheum. 2014;66(6):1421-31. doi: 10.1002/art.38400Felten R, Scher F, Sagez F, et al. Spotlight on anifrolumab and its potential for the treatment of moderate-to-severe systemic lupus erythematosus: evidence to date. Drug Des Devel Ther. 2019;13:1535-43. doi: 10.2147/DDDT.S170969Sanayama Y, Ikeda K, Saito Y, et al. Prediction of therapeutic responses to tocilizumab in patients with rheumatoid arthritis: biomarkers identified by analysis of gene expression in peripheral blood mononuclear cells using genome-wide DNA microarray. Arthritis Rheum. 2014;66(6):1421-31. doi: 10.1002/art.38400Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an antiinterferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheum. 2017;69:376-86. doi: 10.1002/art.39962Sanayama Y, Ikeda K, Saito Y, et al. Prediction of therapeutic responses to tocilizumab in patients with rheumatoid arthritis: biomarkers identified by analysis of gene expression in peripheral blood mononuclear cells using genome-wide DNA microarray. Arthritis Rheum. 2014;66(6):1421-31. doi: 10.1002/art.38400Merrill JT, Furie R, Werth VP, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med. 2018;5(1):e000284. doi: 10.1136/lupus-2018-000284Mavragani CP, La DT, Stohl W, Crow MK. Association of the response to tumor necrosis factor antagonists with plasma type I interferon activity and interferon-β/α ratios in rheumatoid arthritis patients: a post hoc analysis of a predominantly Hispanic cohort. Arthritis Rheum. 2010;62:392-401. doi: 10.1002/art.27226Casey KA, Guo X, Smith MA, et al. Type I interferon receptor blockade with anifrolumab corrects innate and adaptive immune perturbations of SLE. Lupus Sci Med. 2018;5(1):e000286. doi: 10.1136/lupus-2018-000286Mavragani CP, La DT, Stohl W, Crow MK. Association of the response to tumor necrosis factor antagonists with plasma type I interferon activity and interferon-β/α ratios in rheumatoid arthritis patients: a post hoc analysis of a predominantly Hispanic cohort. Arthritis Rheum. 2010;62:392-401. doi: 10.1002/art.27226Goldberg A, Geppert T, Schiopu E, et al. Dose-escalation of human anti-interferon-α receptor monoclonal antibody MEDI-546 in subjects with systemic sclerosis: a phase 1, multicenter, open label study. Arthritis Res Ther. 2014;16:R57.Mavragani CP, La DT, Stohl W, Crow MK. Association of the response to tumor necrosis factor antagonists with plasma type I interferon activity and interferon-β/α ratios in rheumatoid arthritis patients: a post hoc analysis of a predominantly Hispanic cohort. Arthritis Rheum. 2010;62:392-401. doi: 10.1002/art.27226doi: 10.1186/ar4492Wampler Muskardin T, Vashisht P, Dorschner JM, et al. Increased pretreatment serum IFN-β/α ratio predicts non-response to tumour necrosis factor α inhibition in rheumatoid arthritis. Ann Rheum Dis. 2016;75(10):1757-62. doi: 10.1136/annrheumdis-2015-208001Update on TULIP 1 phase III trial for anifrolumab in systemic lupus erythematosus. Available from: https://www.astrazeneca.com/media-centre/press-releases/2018/update-on-tulip-1-phase-iii-trial-for-anifrolumab-insystemic-lupus-erythematosus-31082018.html. Accessed January 10, 2019.Wampler Muskardin T, Vashisht P, Dorschner JM, et al. Increased pretreatment serum IFN-β/α ratio predicts non-response to tumour necrosis factor α inhibition in rheumatoid arthritis. Ann Rheum Dis. 2016;75(10):1757-62. doi: 10.1136/annrheumdis-2015-208001Schwartz DM, Kanno Y, Villarino A, et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-62. doi: 10.1038/nrd.2017.201Wampler Muskardin T, Vashisht P, Dorschner JM, et al. Increased pretreatment serum IFN-β/α ratio predicts non-response to tumour necrosis factor α inhibition in rheumatoid arthritis. Ann Rheum Dis. 2016;75(10):1757-62. doi: 10.1136/annrheumdis-2015-208001Насонов ЕЛ, Лила АМ. Ингибиторы Янус-киназ при иммуновоспалительных ревматических заболеваниях: новые возможности и перспективы. Научно-практическая ревматология. 2019;57(1):8-16 doi: 10.14412/1995-4484-2019-8-16De Jong TD, Blits M, de Ridder S, et al. Type I interferon response gene expression in established rheumatoid arthritis is not associated with clinical parameters. Arthritis Res Ther. 2016;18:Article number 290. doi: 10.1186/s13075-016-1191-yMok CC. The Jakinibs in systemic lupus erythematosus: progress and prospects. Expert Opin Investig Drugs. 2019;28(1):85-92. doi: 10.1080/13543784.2019.1551358De Jong TD, Blits M, de Ridder S, et al. Type I interferon response gene expression in established rheumatoid arthritis is not associated with clinical parameters. Arthritis Res Ther. 2016;18:Article number 290. doi: 10.1186/s13075-016-1191-ySanchez GAM, Reinhardt A, Ramsey S, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;128(7):3041-52. doi: 10.1172/JCI98814De Jong TD, Blits M, de Ridder S, et al. Type I interferon response gene expression in established rheumatoid arthritis is not associated with clinical parameters. Arthritis Res Ther. 2016;18:Article number 290. doi: 10.1186/s13075-016-1191-yKö nig N, Fiehn C, Wolf C, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2017;76(2):468-72.De Jong TD, Vosslamber S, Blits M, et al. Effect of prednisone on type I interferon signature in rheumatoid arthritis: consequences for response prediction to rituximab. Arthritis Res Ther. 2015;17:78. doi: 10.1186/s13075-015-0564-yRodero MP, Fremond M-L, Rice GI, et al. JAK inhibition in STING-associated interferonopathy. Ann Rheum Dis. 2016;75(12):e75. doi: 10.1136/annrheumdis-2016-210504De Jong TD, Vosslamber S, Blits M, et al. Effect of prednisone on type I interferon signature in rheumatoid arthritis: consequences for response prediction to rituximab. Arthritis Res Ther. 2015;17:78. doi: 10.1186/s13075-015-0564-ySeo J, Kang J-A, Suh DI, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139(4):1396-9.e12. doi: 10.1016/j.jaci.2016.10.030De Jong TD, Vosslamber S, Blits M, et al. Effect of prednisone on type I interferon signature in rheumatoid arthritis: consequences for response prediction to rituximab. Arthritis Res Ther. 2015;17:78. doi: 10.1186/s13075-015-0564-yVolpi S, Insalaco A, Caorsi R, et al. Efficacy and Adverse Events During Janus Kinase Inhibitor Treatment of SAVI Syndrome. J Clin Immunol. 2019 Jul;39(5):476-85. doi: 10.1007/s10875-019-00645-0De Jong TD, Snoek T, Mantel E, et al. Dynamics of the Type I Interferon Response During Immunosuppressive Therapy in Rheumatoid Arthritis. Front Immunol. 2019 Apr 24;10:902. doi: 10.3389/fimmu.2019.00902Ikeda K, Hayakawa K, Fujishiro M, et al. JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation. BMC Immunol. 2017;18(1):41. doi: 10.1186/s12865-017-0225-9De Jong TD, Snoek T, Mantel E, et al. Dynamics of the Type I Interferon Response During Immunosuppressive Therapy in Rheumatoid Arthritis. Front Immunol. 2019 Apr 24;10:902. doi: 10.3389/fimmu.2019.00902Furumoto Y, Smith CK, Blanco L, et al. Tofacitinib Ameliorates Murine Lupus and Its Associated Vascular Dysfunction. Arthritis Rheum. 2017;69(1):148-60. doi: 10.1002/art.39818De Jong TD, Snoek T, Mantel E, et al. Dynamics of the Type I Interferon Response During Immunosuppressive Therapy in Rheumatoid Arthritis. Front Immunol. 2019 Apr 24;10:902. doi: 10.3389/fimmu.2019.00902Yamamoto M, Yokoyama Y, Shimizu Y, et al. Tofacitinib can decrease anti-DNA antibody titers in inactive systemic lupus erythematosus complicated by rheumatoid arthritis. Mod Rheumatol. 2016;26(4):633-4. doi: 10.3109/14397595.2015.1069473Thorlacius GE, Wahren-Herlenius M, Ronnblom L. An update on the role of type I interferons in systemic lupus erythematosus and Sjogren's syndrome. Curr Opin Rheumatol. 2018;30:471-81. doi: 10.1097/BOR.0000000000000524You H, Zhang G, Wang Q, et al. Successful treatment of arthritis and rash with tofacitinib in systemic lupus erythematosus: the experience from a single centre. Ann Rheum Dis. 2019 Apr 20. doi: 10.1136/annrheumdis-2019-215455Thorlacius GE, Wahren-Herlenius M, Ronnblom L. An update on the role of type I interferons in systemic lupus erythematosus and Sjogren's syndrome. Curr Opin Rheumatol. 2018;30:471-81. doi: 10.1097/BOR.0000000000000524Wallace DJ, Furie RA, Tanaka Y, et al. Baricitinib for systemic lupus erythematosus: a double-blind, randomised, placebo-controlled, phase 2 trial. Lancet. 2018;392(10143):222-31. doi: 10.1016/S0140-6736(18)31363-1Thorlacius GE, Wahren-Herlenius M, Ronnblom L. An update on the role of type I interferons in systemic lupus erythematosus and Sjogren's syndrome. Curr Opin Rheumatol. 2018;30:471-81. doi: 10.1097/BOR.0000000000000524Zhang LJ. Type 1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis. Front Immunol. 2019;10:1440. doi: 10.3389/fimmu.2019.01440Nezos A, Gravani F, Tassidou A, et al. Type I and II interferon signatures in Sjogren's syndrome pathogenesis: contributions in distinct clinical phenotypes and Sjogren's related lymphomagenesis. J Autoimmun. 2015;63:47-58. doi: 10.1016/j.jaut.2015.07.002Mylonas A, Conrad C. Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon. Front Immunol. 2018;9:2746. doi: 10.3389/fimmu.2018.02746Nezos A, Gravani F, Tassidou A, et al. Type I and II interferon signatures in Sjogren's syndrome pathogenesis: contributions in distinct clinical phenotypes and Sjogren's related lymphomagenesis. J Autoimmun. 2015;63:47-58. doi: 10.1016/j.jaut.2015.07.002Robinson ES, Werth VP. The role of cytokines in the pathogenesis of cutaneous lupus erythematosus. Cytokine. 2015;73:326-34. doi: 10.1016/j.cyto.2015.01.031Nezos A, Gravani F, Tassidou A, et al. Type I and II interferon signatures in Sjogren's syndrome pathogenesis: contributions in distinct clinical phenotypes and Sjogren's related lymphomagenesis. J Autoimmun. 2015;63:47-58. doi: 10.1016/j.jaut.2015.07.002Rubin RL. Drug-induced lupus. Expert Opin Drug Safe. 2015;14:361-78. doi: 10.1517/14740338.2015.995089Benchabane S, Belkhelfa M, Belguendouz H, et al. Interferon-γ inhibits inflammatory responses mediators via suppression of iNOS signaling pathway in PBMCs from patients with primary Sjö gren's syndrome. Inflammopharmacology. 2018;26:1165-74. doi: 10.1007/s10787-018-0499-4Ciechanowicz P, Rakowska A, Sikora M, Rudnicka L. JAKinhibitors in dermatology. Current evidence and future applications. J Dermatolog Treat. 2018 Nov;15:1-22. doi: 10.1080/09546634.2018.1546043Benchabane S, Belkhelfa M, Belguendouz H, et al. Interferon-γ inhibits inflammatory responses mediators via suppression of iNOS signaling pathway in PBMCs from patients with primary Sjö gren's syndrome. Inflammopharmacology. 2018;26:1165-74. doi: 10.1007/s10787-018-0499-4Benchabane S, Belkhelfa M, Belguendouz H, et al. Interferon-γ inhibits inflammatory responses mediators via suppression of iNOS signaling pathway in PBMCs from patients with primary Sjö gren's syndrome. Inflammopharmacology. 2018;26:1165-74. doi: 10.1007/s10787-018-0499-4Benchabane S, Belkhelfa M, Belguendouz H, et al. Interferon-γ inhibits inflammatory responses mediators via suppression of iNOS signaling pathway in PBMCs from patients with primary Sjö gren's syndrome. Inflammopharmacology. 2018;26:1165-74. doi: 10.1007/s10787-018-0499-4Bodewes ILA, Al-Ali S, van Helden-Meeuwsen CG, et al. Systemic interferon type I and type II signatures in primary Sjö gren's syndrome reveal differences in biological disease activity. Rheumatology. 2018;57:921-30. doi: 10.1093/rheumatology/kex490Bodewes ILA, Al-Ali S, van Helden-Meeuwsen CG, et al. Systemic interferon type I and type II signatures in primary Sjö gren's syndrome reveal differences in biological disease activity. Rheumatology. 2018;57:921-30. doi: 10.1093/rheumatology/kex490Bodewes ILA, Al-Ali S, van Helden-Meeuwsen CG, et al. Systemic interferon type I and type II signatures in primary Sjö gren's syndrome reveal differences in biological disease activity. Rheumatology. 2018;57:921-30. doi: 10.1093/rheumatology/kex490Bodewes ILA, Al-Ali S, van Helden-Meeuwsen CG, et al. Systemic interferon type I and type II signatures in primary Sjö gren's syndrome reveal differences in biological disease activity. Rheumatology. 2018;57:921-30. doi: 10.1093/rheumatology/kex490Bodewes ILA, Al-Ali S, van Helden-Meeuwsen CG, et al. Systemic interferon type I and type II signatures in primary Sjö gren's syndrome reveal differences in biological disease activity. Rheumatology. 2018;57:921-30. doi: 10.1093/rheumatology/kex490Bodewes ILA, Al-Ali S, van Helden-Meeuwsen CG, et al. Systemic interferon type I and type II signatures in primary Sjö gren's syndrome reveal differences in biological disease activity. Rheumatology. 2018;57:921-30. doi: 10.1093/rheumatology/kex490Bodewes ILA, Al-Ali S, van Helden-Meeuwsen CG, et al. Systemic interferon type I and type II signatures in primary Sjö gren's syndrome reveal differences in biological disease activity. Rheumatology. 2018;57:921-30. doi: 10.1093/rheumatology/kex490Bodewes ILA, Al-Ali S, van Helden-Meeuwsen CG, et al. Systemic interferon type I and type II signatures in primary Sjö gren's syndrome reveal differences in biological disease activity. Rheumatology. 2018;57:921-30. doi: 10.1093/rheumatology/kex490Dieude P, Guedj M, Wipff J, et al. STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. Arthritis Rheum. 2009;60:2472-9. doi: 10.1002/art.24688Dieude P, Guedj M, Wipff J, et al. STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. Arthritis Rheum. 2009;60:2472-9. doi: 10.1002/art.24688Dieude P, Guedj M, Wipff J, et al. STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. Arthritis Rheum. 2009;60:2472-9. doi: 10.1002/art.24688Dieude P, Guedj M, Wipff J, et al. STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. Arthritis Rheum. 2009;60:2472-9. doi: 10.1002/art.24688Dieude P, Guedj M, Wipff J, et al. STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. Arthritis Rheum. 2009;60:2472-9. doi: 10.1002/art.24688Dieude P, Guedj M, Wipff J, et al. STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. Arthritis Rheum. 2009;60:2472-9. doi: 10.1002/art.24688Dieude P, Guedj M, Wipff J, et al. STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. Arthritis Rheum. 2009;60:2472-9. doi: 10.1002/art.24688Dieude P, Guedj M, Wipff J, et al. STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. Arthritis Rheum. 2009;60:2472-9. doi: 10.1002/art.24688Gourh P, Agarwal SK, Divecha D, et al. Polymorphisms in TBX21 and STAT4 increase the risk of systemic sclerosis: evidence of possible gene-gene interaction and alterations in Th1/Th2 cytokines. Arthritis Rheum. 2009;60:3794-806. doi: 10.1002/art.24958Gourh P, Agarwal SK, Divecha D, et al. Polymorphisms in TBX21 and STAT4 increase the risk of systemic sclerosis: evidence of possible gene-gene interaction and alterations in Th1/Th2 cytokines. Arthritis Rheum. 2009;60:3794-806. doi: 10.1002/art.24958Gourh P, Agarwal SK, Divecha D, et al. Polymorphisms in TBX21 and STAT4 increase the risk of systemic sclerosis: evidence of possible gene-gene interaction and alterations in Th1/Th2 cytokines. Arthritis Rheum. 2009;60:3794-806. doi: 10.1002/art.24958Gourh P, Agarwal SK, Divecha D, et al. Polymorphisms in TBX21 and STAT4 increase the risk of systemic sclerosis: evidence of possible gene-gene interaction and alterations in Th1/Th2 cytokines. Arthritis Rheum. 2009;60:3794-806. doi: 10.1002/art.24958Gourh P, Agarwal SK, Divecha D, et al. Polymorphisms in TBX21 and STAT4 increase the risk of systemic sclerosis: evidence of possible gene-gene interaction and alterations in Th1/Th2 cytokines. Arthritis Rheum. 2009;60:3794-806. doi: 10.1002/art.24958Gourh P, Agarwal SK, Divecha D, et al. Polymorphisms in TBX21 and STAT4 increase the risk of systemic sclerosis: evidence of possible gene-gene interaction and alterations in Th1/Th2 cytokines. Arthritis Rheum. 2009;60:3794-806. doi: 10.1002/art.24958Gourh P, Agarwal SK, Divecha D, et al. Polymorphisms in TBX21 and STAT4 increase the risk of systemic sclerosis: evidence of possible gene-gene interaction and alterations in Th1/Th2 cytokines. Arthritis Rheum. 2009;60:3794-806. doi: 10.1002/art.24958Gourh P, Agarwal SK, Divecha D, et al. Polymorphisms in TBX21 and STAT4 increase the risk of systemic sclerosis: evidence of possible gene-gene interaction and alterations in Th1/Th2 cytokines. Arthritis Rheum. 2009;60:3794-806. doi: 10.1002/art.24958Rueda B, Broen J, Simeon C, et al. The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype. Hum Mol Genet. 2009;18:2071-7. doi: 10.1093/hmg/ddp119Rueda B, Broen J, Simeon C, et al. The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype. Hum Mol Genet. 2009;18:2071-7. doi: 10.1093/hmg/ddp119Rueda B, Broen J, Simeon C, et al. The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype. Hum Mol Genet. 2009;18:2071-7. doi: 10.1093/hmg/ddp119Rueda B, Broen J, Simeon C, et al. The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype. Hum Mol Genet. 2009;18:2071-7. doi: 10.1093/hmg/ddp119Rueda B, Broen J, Simeon C, et al. The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype. Hum Mol Genet. 2009;18:2071-7. doi: 10.1093/hmg/ddp119Rueda B, Broen J, Simeon C, et al. The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype. Hum Mol Genet. 2009;18:2071-7. doi: 10.1093/hmg/ddp119Rueda B, Broen J, Simeon C, et al. The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype. Hum Mol Genet. 2009;18:2071-7. doi: 10.1093/hmg/ddp119Rueda B, Broen J, Simeon C, et al. The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype. Hum Mol Genet. 2009;18:2071-7. doi: 10.1093/hmg/ddp119Skaug B, Assassi S. Type I interferon dysregulation in Systemic Sclerosis. Cytokine. 2019 Jan 23. doi: 10.1016/j.cyto.2018.12.018Skaug B, Assassi S. Type I interferon dysregulation in Systemic Sclerosis. Cytokine. 2019 Jan 23. doi: 10.1016/j.cyto.2018.12.018Skaug B, Assassi S. Type I interferon dysregulation in Systemic Sclerosis. Cytokine. 2019 Jan 23. doi: 10.1016/j.cyto.2018.12.018Skaug B, Assassi S. Type I interferon dysregulation in Systemic Sclerosis. Cytokine. 2019 Jan 23. doi: 10.1016/j.cyto.2018.12.018Skaug B, Assassi S. Type I interferon dysregulation in Systemic Sclerosis. Cytokine. 2019 Jan 23. doi: 10.1016/j.cyto.2018.12.018Skaug B, Assassi S. Type I interferon dysregulation in Systemic Sclerosis. Cytokine. 2019 Jan 23. doi: 10.1016/j.cyto.2018.12.018Skaug B, Assassi S. Type I interferon dysregulation in Systemic Sclerosis. Cytokine. 2019 Jan 23. doi: 10.1016/j.cyto.2018.12.018Skaug B, Assassi S. Type I interferon dysregulation in Systemic Sclerosis. Cytokine. 2019 Jan 23. doi: 10.1016/j.cyto.2018.12.018Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis. Arthritis Rheum. 2014;66:714-25. doi: 10.1002/art.38288Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis. Arthritis Rheum. 2014;66:714-25. doi: 10.1002/art.38288Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis. Arthritis Rheum. 2014;66:714-25. doi: 10.1002/art.38288Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis. Arthritis Rheum. 2014;66:714-25. doi: 10.1002/art.38288Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis. Arthritis Rheum. 2014;66:714-25. doi: 10.1002/art.38288Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis. Arthritis Rheum. 2014;66:714-25. doi: 10.1002/art.38288Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis. Arthritis Rheum. 2014;66:714-25. doi: 10.1002/art.38288Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis. Arthritis Rheum. 2014;66:714-25. doi: 10.1002/art.38288George PM, Oliver E, Dorfmuller P, et al. Evidence for the involvement of type I interferon in pulmonary arterial hypertension. Circ Res. 2014;114:677-88. doi: 10.1161/CIRCRESAHA.114.302221George PM, Oliver E, Dorfmuller P, et al. Evidence for the involvement of type I interferon in pulmonary arterial hypertension. Circ Res. 2014;114:677-88. doi: 10.1161/CIRCRESAHA.114.302221George PM, Oliver E, Dorfmuller P, et al. Evidence for the involvement of type I interferon in pulmonary arterial hypertension. Circ Res. 2014;114:677-88. doi: 10.1161/CIRCRESAHA.114.302221George PM, Oliver E, Dorfmuller P, et al. Evidence for the involvement of type I interferon in pulmonary arterial hypertension. Circ Res. 2014;114:677-88. doi: 10.1161/CIRCRESAHA.114.302221George PM, Oliver E, Dorfmuller P, et al. Evidence for the involvement of type I interferon in pulmonary arterial hypertension. Circ Res. 2014;114:677-88. doi: 10.1161/CIRCRESAHA.114.302221George PM, Oliver E, Dorfmuller P, et al. Evidence for the involvement of type I interferon in pulmonary arterial hypertension. Circ Res. 2014;114:677-88. doi: 10.1161/CIRCRESAHA.114.302221George PM, Oliver E, Dorfmuller P, et al. Evidence for the involvement of type I interferon in pulmonary arterial hypertension. Circ Res. 2014;114:677-88. doi: 10.1161/CIRCRESAHA.114.302221George PM, Oliver E, Dorfmuller P, et al. Evidence for the involvement of type I interferon in pulmonary arterial hypertension. Circ Res. 2014;114:677-88. doi: 10.1161/CIRCRESAHA.114.302221Brkic Z, van Bon L, Cossu M, et al. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis. Ann Rheum Dis. 2016;75(8):1567-73. doi: 10.1136/annrheumdis-2015-207Brkic Z, van Bon L, Cossu M, et al. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis. Ann Rheum Dis. 2016;75(8):1567-73. doi: 10.1136/annrheumdis-2015-207Brkic Z, van Bon L, Cossu M, et al. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis. Ann Rheum Dis. 2016;75(8):1567-73. doi: 10.1136/annrheumdis-2015-207Brkic Z, van Bon L, Cossu M, et al. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis. Ann Rheum Dis. 2016;75(8):1567-73. doi: 10.1136/annrheumdis-2015-207Brkic Z, van Bon L, Cossu M, et al. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis. Ann Rheum Dis. 2016;75(8):1567-73. doi: 10.1136/annrheumdis-2015-207Brkic Z, van Bon L, Cossu M, et al. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis. Ann Rheum Dis. 2016;75(8):1567-73. doi: 10.1136/annrheumdis-2015-207Brkic Z, van Bon L, Cossu M, et al. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis. Ann Rheum Dis. 2016;75(8):1567-73. doi: 10.1136/annrheumdis-2015-207Brkic Z, van Bon L, Cossu M, et al. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis. Ann Rheum Dis. 2016;75(8):1567-73. doi: 10.1136/annrheumdis-2015-207Van den Hoogen LL, Fritsch-Stork RD, Versnel MA, et al. Monocyte type I interferon signature in antiphospholipid syndrome is related to proinflammatory monocyte subsets, hydroxychloroquine and statin use. Ann Rheum Dis. 2016;75:e81. doi: 10.1136/annrheumdis-2016-210485Van den Hoogen LL, Fritsch-Stork RD, Versnel MA, et al. Monocyte type I interferon signature in antiphospholipid syndrome is related to proinflammatory monocyte subsets, hydroxychloroquine and statin use. Ann Rheum Dis. 2016;75:e81. doi: 10.1136/annrheumdis-2016-210485Van den Hoogen LL, Fritsch-Stork RD, Versnel MA, et al. Monocyte type I interferon signature in antiphospholipid syndrome is related to proinflammatory monocyte subsets, hydroxychloroquine and statin use. Ann Rheum Dis. 2016;75:e81. doi: 10.1136/annrheumdis-2016-210485Van den Hoogen LL, Fritsch-Stork RD, Versnel MA, et al. Monocyte type I interferon signature in antiphospholipid syndrome is related to proinflammatory monocyte subsets, hydroxychloroquine and statin use. Ann Rheum Dis. 2016;75:e81. doi: 10.1136/annrheumdis-2016-210485Van den Hoogen LL, Fritsch-Stork RD, Versnel MA, et al. Monocyte type I interferon signature in antiphospholipid syndrome is related to proinflammatory monocyte subsets, hydroxychloroquine and statin use. Ann Rheum Dis. 2016;75:e81. doi: 10.1136/annrheumdis-2016-210485Van den Hoogen LL, Fritsch-Stork RD, Versnel MA, et al. Monocyte type I interferon signature in antiphospholipid syndrome is related to proinflammatory monocyte subsets, hydroxychloroquine and statin use. Ann Rheum Dis. 2016;75:e81. doi: 10.1136/annrheumdis-2016-210485Van den Hoogen LL, Fritsch-Stork RD, Versnel MA, et al. Monocyte type I interferon signature in antiphospholipid syndrome is related to proinflammatory monocyte subsets, hydroxychloroquine and statin use. Ann Rheum Dis. 2016;75:e81. doi: 10.1136/annrheumdis-2016-210485Van den Hoogen LL, Fritsch-Stork RD, Versnel MA, et al. Monocyte type I interferon signature in antiphospholipid syndrome is related to proinflammatory monocyte subsets, hydroxychloroquine and statin use. Ann Rheum Dis. 2016;75:e81. doi: 10.1136/annrheumdis-2016-210485Ugolini-Lopes MR, Torrezan GT, Gandara APR, et al. Enhanced type I interferon gene signature in primary antiphospholipid syndrome: Association with earlier disease onset and preeclampsia. Autoimmun Rev. 2019;18(4):393-8. doi: 10.1016/j.autrev.2018.11.004Ugolini-Lopes MR, Torrezan GT, Gandara APR, et al. Enhanced type I interferon gene signature in primary antiphospholipid syndrome: Association with earlier disease onset and preeclampsia. Autoimmun Rev. 2019;18(4):393-8. doi: 10.1016/j.autrev.2018.11.004Ugolini-Lopes MR, Torrezan GT, Gandara APR, et al. Enhanced type I interferon gene signature in primary antiphospholipid syndrome: Association with earlier disease onset and preeclampsia. Autoimmun Rev. 2019;18(4):393-8. doi: 10.1016/j.autrev.2018.11.004Ugolini-Lopes MR, Torrezan GT, Gandara APR, et al. Enhanced type I interferon gene signature in primary antiphospholipid syndrome: Association with earlier disease onset and preeclampsia. Autoimmun Rev. 2019;18(4):393-8. doi: 10.1016/j.autrev.2018.11.004Ugolini-Lopes MR, Torrezan GT, Gandara APR, et al. Enhanced type I interferon gene signature in primary antiphospholipid syndrome: Association with earlier disease onset and preeclampsia. Autoimmun Rev. 2019;18(4):393-8. doi: 10.1016/j.autrev.2018.11.004Ugolini-Lopes MR, Torrezan GT, Gandara APR, et al. Enhanced type I interferon gene signature in primary antiphospholipid syndrome: Association with earlier disease onset and preeclampsia. Autoimmun Rev. 2019;18(4):393-8. doi: 10.1016/j.autrev.2018.11.004Ugolini-Lopes MR, Torrezan GT, Gandara APR, et al. Enhanced type I interferon gene signature in primary antiphospholipid syndrome: Association with earlier disease onset and preeclampsia. Autoimmun Rev. 2019;18(4):393-8. doi: 10.1016/j.autrev.2018.11.004Ugolini-Lopes MR, Torrezan GT, Gandara APR, et al. Enhanced type I interferon gene signature in primary antiphospholipid syndrome: Association with earlier disease onset and preeclampsia. Autoimmun Rev. 2019;18(4):393-8. doi: 10.1016/j.autrev.2018.11.004Palli E, Kravvariti E, Tektonidou MG. Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations. Front Immunol. 2019;10:487. doi: 10.3389/fimmu.2019.00487Palli E, Kravvariti E, Tektonidou MG. Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations. Front Immunol. 2019;10:487. doi: 10.3389/fimmu.2019.00487Palli E, Kravvariti E, Tektonidou MG. Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations. Front Immunol. 2019;10:487. doi: 10.3389/fimmu.2019.00487Palli E, Kravvariti E, Tektonidou MG. Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations. Front Immunol. 2019;10:487. doi: 10.3389/fimmu.2019.00487Palli E, Kravvariti E, Tektonidou MG. Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations. Front Immunol. 2019;10:487. doi: 10.3389/fimmu.2019.00487Palli E, Kravvariti E, Tektonidou MG. Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations. Front Immunol. 2019;10:487. doi: 10.3389/fimmu.2019.00487Palli E, Kravvariti E, Tektonidou MG. Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations. Front Immunol. 2019;10:487. doi: 10.3389/fimmu.2019.00487Palli E, Kravvariti E, Tektonidou MG. Type I Interferon Signature in Primary Antiphospholipid Syndrome: Clinical and Laboratory Associations. Front Immunol. 2019;10:487. doi: 10.3389/fimmu.2019.00487Grenn RC, Yalavarthi S, Gandhi AA, et al. Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome. Ann Rheum Dis. 2017;76:450-7. doi: 10.1136/annrheumdis-2016-209442Grenn RC, Yalavarthi S, Gandhi AA, et al. Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome. Ann Rheum Dis. 2017;76:450-7. doi: 10.1136/annrheumdis-2016-209442Grenn RC, Yalavarthi S, Gandhi AA, et al. Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome. Ann Rheum Dis. 2017;76:450-7. doi: 10.1136/annrheumdis-2016-209442Grenn RC, Yalavarthi S, Gandhi AA, et al. Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome. Ann Rheum Dis. 2017;76:450-7. doi: 10.1136/annrheumdis-2016-209442Grenn RC, Yalavarthi S, Gandhi AA, et al. Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome. Ann Rheum Dis. 2017;76:450-7. doi: 10.1136/annrheumdis-2016-209442Grenn RC, Yalavarthi S, Gandhi AA, et al. Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome. Ann Rheum Dis. 2017;76:450-7. doi: 10.1136/annrheumdis-2016-209442Grenn RC, Yalavarthi S, Gandhi AA, et al. Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome. Ann Rheum Dis. 2017;76:450-7. doi: 10.1136/annrheumdis-2016-209442Grenn RC, Yalavarthi S, Gandhi AA, et al. Endothelial progenitor dysfunction associates with a type I interferon signature in primary antiphospholipid syndrome. Ann Rheum Dis. 2017;76:450-7. doi: 10.1136/annrheumdis-2016-209442Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-β/α-mediated innate immune mechanisms in dermatomyositis. Ann Neurol. 2005;57:664-78. doi: 10.1002/ana.20464Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-β/α-mediated innate immune mechanisms in dermatomyositis. Ann Neurol. 2005;57:664-78. doi: 10.1002/ana.20464Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-β/α-mediated innate immune mechanisms in dermatomyositis. Ann Neurol. 2005;57:664-78. doi: 10.1002/ana.20464Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-β/α-mediated innate immune mechanisms in dermatomyositis. Ann Neurol. 2005;57:664-78. doi: 10.1002/ana.20464Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-β/α-mediated innate immune mechanisms in dermatomyositis. Ann Neurol. 2005;57:664-78. doi: 10.1002/ana.20464Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-β/α-mediated innate immune mechanisms in dermatomyositis. Ann Neurol. 2005;57:664-78. doi: 10.1002/ana.20464Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-β/α-mediated innate immune mechanisms in dermatomyositis. Ann Neurol. 2005;57:664-78. doi: 10.1002/ana.20464Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-β/α-mediated innate immune mechanisms in dermatomyositis. Ann Neurol. 2005;57:664-78. doi: 10.1002/ana.20464Liao AP, Salajegheh M, Nazareno R, et al. Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis. Ann Rheum Dis. 2011;70:831-6. doi: 10.1136/ard.2010.139949Liao AP, Salajegheh M, Nazareno R, et al. Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis. Ann Rheum Dis. 2011;70:831-6. doi: 10.1136/ard.2010.139949Liao AP, Salajegheh M, Nazareno R, et al. Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis. Ann Rheum Dis. 2011;70:831-6. doi: 10.1136/ard.2010.139949Liao AP, Salajegheh M, Nazareno R, et al. Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis. Ann Rheum Dis. 2011;70:831-6. doi: 10.1136/ard.2010.139949Liao AP, Salajegheh M, Nazareno R, et al. Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis. Ann Rheum Dis. 2011;70:831-6. doi: 10.1136/ard.2010.139949Liao AP, Salajegheh M, Nazareno R, et al. Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis. Ann Rheum Dis. 2011;70:831-6. doi: 10.1136/ard.2010.139949Liao AP, Salajegheh M, Nazareno R, et al. Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis. Ann Rheum Dis. 2011;70:831-6. doi: 10.1136/ard.2010.139949Liao AP, Salajegheh M, Nazareno R, et al. Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis. Ann Rheum Dis. 2011;70:831-6. doi: 10.1136/ard.2010.139949Somani A-K, Swick AR, Cooper KD, et al. Severe dermatomyositis triggered by interferon beta-1a therapy and associated with enhanced type I interferon signaling. Arch Dermatol. 2008;144:1341-9. doi: 10.1001/archderm.144.10.1341Somani A-K, Swick AR, Cooper KD, et al. Severe dermatomyositis triggered by interferon beta-1a therapy and associated with enhanced type I interferon signaling. Arch Dermatol. 2008;144:1341-9. doi: 10.1001/archderm.144.10.1341Somani A-K, Swick AR, Cooper KD, et al. Severe dermatomyositis triggered by interferon beta-1a therapy and associated with enhanced type I interferon signaling. Arch Dermatol. 2008;144:1341-9. doi: 10.1001/archderm.144.10.1341Somani A-K, Swick AR, Cooper KD, et al. Severe dermatomyositis triggered by interferon beta-1a therapy and associated with enhanced type I interferon signaling. Arch Dermatol. 2008;144:1341-9. doi: 10.1001/archderm.144.10.1341Somani A-K, Swick AR, Cooper KD, et al. Severe dermatomyositis triggered by interferon beta-1a therapy and associated with enhanced type I interferon signaling. Arch Dermatol. 2008;144:1341-9. doi: 10.1001/archderm.144.10.1341Somani A-K, Swick AR, Cooper KD, et al. Severe dermatomyositis triggered by interferon beta-1a therapy and associated with enhanced type I interferon signaling. Arch Dermatol. 2008;144:1341-9. doi: 10.1001/archderm.144.10.1341Somani A-K, Swick AR, Cooper KD, et al. Severe dermatomyositis triggered by interferon beta-1a therapy and associated with enhanced type I interferon signaling. Arch Dermatol. 2008;144:1341-9. doi: 10.1001/archderm.144.10.1341Somani A-K, Swick AR, Cooper KD, et al. Severe dermatomyositis triggered by interferon beta-1a therapy and associated with enhanced type I interferon signaling. Arch Dermatol. 2008;144:1341-9. doi: 10.1001/archderm.144.10.1341Piper CJM, Wilkinson MGL, Deakin CT, et al. CD19+CD24hiCD38hi B Cells Are Expanded in Juvenile Dermatomyositis and Exhibit a Pro-Inflammatory Phenotype After Activation Through Toll-Like Receptor 7 and Interferon-α. Front Immunol. 2018;9. doi: 10.3389/fimmu.2018.01372Piper CJM, Wilkinson MGL, Deakin CT, et al. CD19+CD24hiCD38hi B Cells Are Expanded in Juvenile Dermatomyositis and Exhibit a Pro-Inflammatory Phenotype After Activation Through Toll-Like Receptor 7 and Interferon-α. Front Immunol. 2018;9. doi: 10.3389/fimmu.2018.01372Piper CJM, Wilkinson MGL, Deakin CT, et al. CD19+CD24hiCD38hi B Cells Are Expanded in Juvenile Dermatomyositis and Exhibit a Pro-Inflammatory Phenotype After Activation Through Toll-Like Receptor 7 and Interferon-α. Front Immunol. 2018;9. doi: 10.3389/fimmu.2018.01372Piper CJM, Wilkinson MGL, Deakin CT, et al. CD19+CD24hiCD38hi B Cells Are Expanded in Juvenile Dermatomyositis and Exhibit a Pro-Inflammatory Phenotype After Activation Through Toll-Like Receptor 7 and Interferon-α. Front Immunol. 2018;9. doi: 10.3389/fimmu.2018.01372Piper CJM, Wilkinson MGL, Deakin CT, et al. CD19+CD24hiCD38hi B Cells Are Expanded in Juvenile Dermatomyositis and Exhibit a Pro-Inflammatory Phenotype After Activation Through Toll-Like Receptor 7 and Interferon-α. Front Immunol. 2018;9. doi: 10.3389/fimmu.2018.01372Piper CJM, Wilkinson MGL, Deakin CT, et al. CD19+CD24hiCD38hi B Cells Are Expanded in Juvenile Dermatomyositis and Exhibit a Pro-Inflammatory Phenotype After Activation Through Toll-Like Receptor 7 and Interferon-α. Front Immunol. 2018;9. doi: 10.3389/fimmu.2018.01372Piper CJM, Wilkinson MGL, Deakin CT, et al. CD19+CD24hiCD38hi B Cells Are Expanded in Juvenile Dermatomyositis and Exhibit a Pro-Inflammatory Phenotype After Activation Through Toll-Like Receptor 7 and Interferon-α. Front Immunol. 2018;9. doi: 10.3389/fimmu.2018.01372Piper CJM, Wilkinson MGL, Deakin CT, et al. CD19+CD24hiCD38hi B Cells Are Expanded in Juvenile Dermatomyositis and Exhibit a Pro-Inflammatory Phenotype After Activation Through Toll-Like Receptor 7 and Interferon-α. Front Immunol. 2018;9. doi: 10.3389/fimmu.2018.01372Oon S, Wilson NJ, Wicks I. Targeted therapeutics in SLE: emerging strategies to modulate the interferon pathway. Clin Transl Immunol. 2016;5:e79. doi: 10.1038/cti.2016.26Oon S, Wilson NJ, Wicks I. Targeted therapeutics in SLE: emerging strategies to modulate the interferon pathway. Clin Transl Immunol. 2016;5:e79. doi: 10.1038/cti.2016.26Oon S, Wilson NJ, Wicks I. Targeted therapeutics in SLE: emerging strategies to modulate the interferon pathway. Clin Transl Immunol. 2016;5:e79. doi: 10.1038/cti.2016.26Oon S, Wilson NJ, Wicks I. Targeted therapeutics in SLE: emerging strategies to modulate the interferon pathway. Clin Transl Immunol. 2016;5:e79. doi: 10.1038/cti.2016.26Oon S, Wilson NJ, Wicks I. Targeted therapeutics in SLE: emerging strategies to modulate the interferon pathway. Clin Transl Immunol. 2016;5:e79. doi: 10.1038/cti.2016.26Oon S, Wilson NJ, Wicks I. Targeted therapeutics in SLE: emerging strategies to modulate the interferon pathway. Clin Transl Immunol. 2016;5:e79. doi: 10.1038/cti.2016.26Oon S, Wilson NJ, Wicks I. Targeted therapeutics in SLE: emerging strategies to modulate the interferon pathway. Clin Transl Immunol. 2016;5:e79. doi: 10.1038/cti.2016.26Oon S, Wilson NJ, Wicks I. Targeted therapeutics in SLE: emerging strategies to modulate the interferon pathway. Clin Transl Immunol. 2016;5:e79. doi: 10.1038/cti.2016.26Mathian A, Hie M, Cohen-Aubart F, et al. Targeting interferons in systemic lupus erythematosus: current and future prospects. Drugs. 2015;75:835-46. doi: 10.1007/s40265-015-0394-xMathian A, Hie M, Cohen-Aubart F, et al. Targeting interferons in systemic lupus erythematosus: current and future prospects. Drugs. 2015;75:835-46. doi: 10.1007/s40265-015-0394-xMathian A, Hie M, Cohen-Aubart F, et al. Targeting interferons in systemic lupus erythematosus: current and future prospects. Drugs. 2015;75:835-46. doi: 10.1007/s40265-015-0394-xMathian A, Hie M, Cohen-Aubart F, et al. Targeting interferons in systemic lupus erythematosus: current and future prospects. Drugs. 2015;75:835-46. doi: 10.1007/s40265-015-0394-xMathian A, Hie M, Cohen-Aubart F, et al. Targeting interferons in systemic lupus erythematosus: current and future prospects. Drugs. 2015;75:835-46. doi: 10.1007/s40265-015-0394-xMathian A, Hie M, Cohen-Aubart F, et al. Targeting interferons in systemic lupus erythematosus: current and future prospects. Drugs. 2015;75:835-46. doi: 10.1007/s40265-015-0394-xMathian A, Hie M, Cohen-Aubart F, et al. Targeting interferons in systemic lupus erythematosus: current and future prospects. Drugs. 2015;75:835-46. doi: 10.1007/s40265-015-0394-xMathian A, Hie M, Cohen-Aubart F, et al. Targeting interferons in systemic lupus erythematosus: current and future prospects. Drugs. 2015;75:835-46. doi: 10.1007/s40265-015-0394-xBodewes ILA, Gottenberg JE, van Helden-Meeuwsen CG, et al. Hydroxychloroquine treatment downregulates systemic interferon activation in primary Sjö gren's syndrome in the JOQUER randomized trial. Rheumatology (Oxford). 2019 Jun 25. doi: 10.1093/rheumatology/kez242Bodewes ILA, Gottenberg JE, van Helden-Meeuwsen CG, et al. Hydroxychloroquine treatment downregulates systemic interferon activation in primary Sjö gren's syndrome in the JOQUER randomized trial. Rheumatology (Oxford). 2019 Jun 25. doi: 10.1093/rheumatology/kez242Bodewes ILA, Gottenberg JE, van Helden-Meeuwsen CG, et al. Hydroxychloroquine treatment downregulates systemic interferon activation in primary Sjö gren's syndrome in the JOQUER randomized trial. Rheumatology (Oxford). 2019 Jun 25. doi: 10.1093/rheumatology/kez242Bodewes ILA, Gottenberg JE, van Helden-Meeuwsen CG, et al. Hydroxychloroquine treatment downregulates systemic interferon activation in primary Sjö gren's syndrome in the JOQUER randomized trial. Rheumatology (Oxford). 2019 Jun 25. doi: 10.1093/rheumatology/kez242Bodewes ILA, Gottenberg JE, van Helden-Meeuwsen CG, et al. Hydroxychloroquine treatment downregulates systemic interferon activation in primary Sjö gren's syndrome in the JOQUER randomized trial. Rheumatology (Oxford). 2019 Jun 25. doi: 10.1093/rheumatology/kez242Bodewes ILA, Gottenberg JE, van Helden-Meeuwsen CG, et al. Hydroxychloroquine treatment downregulates systemic interferon activation in primary Sjö gren's syndrome in the JOQUER randomized trial. Rheumatology (Oxford). 2019 Jun 25. doi: 10.1093/rheumatology/kez242Bodewes ILA, Gottenberg JE, van Helden-Meeuwsen CG, et al. Hydroxychloroquine treatment downregulates systemic interferon activation in primary Sjö gren's syndrome in the JOQUER randomized trial. Rheumatology (Oxford). 2019 Jun 25. doi: 10.1093/rheumatology/kez242Bodewes ILA, Gottenberg JE, van Helden-Meeuwsen CG, et al. Hydroxychloroquine treatment downregulates systemic interferon activation in primary Sjö gren's syndrome in the JOQUER randomized trial. Rheumatology (Oxford). 2019 Jun 25. doi: 10.1093/rheumatology/kez242Gardet A, Pellerin A, McCarl CA, et al. Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNγ Production From Patients Affected With Cutaneous Lupus Erythematosus. Front Immunol. 2019;10:275. doi: 10.3389/fimmu.2019.00275Gardet A, Pellerin A, McCarl CA, et al. Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNγ Production From Patients Affected With Cutaneous Lupus Erythematosus. Front Immunol. 2019;10:275. doi: 10.3389/fimmu.2019.00275Gardet A, Pellerin A, McCarl CA, et al. Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNγ Production From Patients Affected With Cutaneous Lupus Erythematosus. Front Immunol. 2019;10:275. doi: 10.3389/fimmu.2019.00275Gardet A, Pellerin A, McCarl CA, et al. Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNγ Production From Patients Affected With Cutaneous Lupus Erythematosus. Front Immunol. 2019;10:275. doi: 10.3389/fimmu.2019.00275Gardet A, Pellerin A, McCarl CA, et al. Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNγ Production From Patients Affected With Cutaneous Lupus Erythematosus. Front Immunol. 2019;10:275. doi: 10.3389/fimmu.2019.00275Gardet A, Pellerin A, McCarl CA, et al. Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNγ Production From Patients Affected With Cutaneous Lupus Erythematosus. Front Immunol. 2019;10:275. doi: 10.3389/fimmu.2019.00275Gardet A, Pellerin A, McCarl CA, et al. Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNγ Production From Patients Affected With Cutaneous Lupus Erythematosus. Front Immunol. 2019;10:275. doi: 10.3389/fimmu.2019.00275Gardet A, Pellerin A, McCarl CA, et al. Effect of in vivo Hydroxychloroquine and ex vivo Anti-BDCA2 mAb Treatment on pDC IFNγ Production From Patients Affected With Cutaneous Lupus Erythematosus. Front Immunol. 2019;10:275. doi: 10.3389/fimmu.2019.00275Olsen NJ, McAloose C, Carter J, et al. Clinical and Immunologic Profiles in Incomplete Lupus Erythematosus and Improvement with Hydroxychloroquine Treatment. Autoimmune Dis. 2016:8791629. doi: 10.1155/2016/8791629Olsen NJ, McAloose C, Carter J, et al. Clinical and Immunologic Profiles in Incomplete Lupus Erythematosus and Improvement with Hydroxychloroquine Treatment. Autoimmune Dis. 2016:8791629. doi: 10.1155/2016/8791629Olsen NJ, McAloose C, Carter J, et al. Clinical and Immunologic Profiles in Incomplete Lupus Erythematosus and Improvement with Hydroxychloroquine Treatment. Autoimmune Dis. 2016:8791629. doi: 10.1155/2016/8791629Olsen NJ, McAloose C, Carter J, et al. Clinical and Immunologic Profiles in Incomplete Lupus Erythematosus and Improvement with Hydroxychloroquine Treatment. Autoimmune Dis. 2016:8791629. doi: 10.1155/2016/8791629Olsen NJ, McAloose C, Carter J, et al. Clinical and Immunologic Profiles in Incomplete Lupus Erythematosus and Improvement with Hydroxychloroquine Treatment. Autoimmune Dis. 2016:8791629. doi: 10.1155/2016/8791629Olsen NJ, McAloose C, Carter J, et al. Clinical and Immunologic Profiles in Incomplete Lupus Erythematosus and Improvement with Hydroxychloroquine Treatment. Autoimmune Dis. 2016:8791629. doi: 10.1155/2016/8791629Olsen NJ, McAloose C, Carter J, et al. Clinical and Immunologic Profiles in Incomplete Lupus Erythematosus and Improvement with Hydroxychloroquine Treatment. Autoimmune Dis. 2016:8791629. doi: 10.1155/2016/8791629Olsen NJ, McAloose C, Carter J, et al. Clinical and Immunologic Profiles in Incomplete Lupus Erythematosus and Improvement with Hydroxychloroquine Treatment. Autoimmune Dis. 2016:8791629. doi: 10.1155/2016/8791629Eloranta ML, Lö vgren T, Finke D, et al. Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells. Arthritis Rheum. 2009;60:2418-27. doi: 10.1002/art.24686Eloranta ML, Lö vgren T, Finke D, et al. Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells. Arthritis Rheum. 2009;60:2418-27. doi: 10.1002/art.24686Eloranta ML, Lö vgren T, Finke D, et al. Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells. Arthritis Rheum. 2009;60:2418-27. doi: 10.1002/art.24686Eloranta ML, Lö vgren T, Finke D, et al. Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells. Arthritis Rheum. 2009;60:2418-27. doi: 10.1002/art.24686Eloranta ML, Lö vgren T, Finke D, et al. Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells. Arthritis Rheum. 2009;60:2418-27. doi: 10.1002/art.24686Eloranta ML, Lö vgren T, Finke D, et al. Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells. Arthritis Rheum. 2009;60:2418-27. doi: 10.1002/art.24686Eloranta ML, Lö vgren T, Finke D, et al. Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells. Arthritis Rheum. 2009;60:2418-27. doi: 10.1002/art.24686Eloranta ML, Lö vgren T, Finke D, et al. Regulation of the interferon-alpha production induced by RNA-containing immune complexes in plasmacytoid dendritic cells. Arthritis Rheum. 2009;60:2418-27. doi: 10.1002/art.24686Berggren O, Hagberg N, Weber G, et al. B lymphocytes enhance the interferon-alpha production by plasmacytoid dendritic cells. Arthritis Rheum. 2012;64:3409-19.Berggren O, Hagberg N, Weber G, et al. B lymphocytes enhance the interferon-alpha production by plasmacytoid dendritic cells. Arthritis Rheum. 2012;64:3409-19.Berggren O, Hagberg N, Weber G, et al. B lymphocytes enhance the interferon-alpha production by plasmacytoid dendritic cells. Arthritis Rheum. 2012;64:3409-19.Berggren O, Hagberg N, Weber G, et al. B lymphocytes enhance the interferon-alpha production by plasmacytoid dendritic cells. Arthritis Rheum. 2012;64:3409-19.Berggren O, Hagberg N, Weber G, et al. B lymphocytes enhance the interferon-alpha production by plasmacytoid dendritic cells. Arthritis Rheum. 2012;64:3409-19.Berggren O, Hagberg N, Weber G, et al. B lymphocytes enhance the interferon-alpha production by plasmacytoid dendritic cells. Arthritis Rheum. 2012;64:3409-19.Berggren O, Hagberg N, Weber G, et al. B lymphocytes enhance the interferon-alpha production by plasmacytoid dendritic cells. Arthritis Rheum. 2012;64:3409-19.Berggren O, Hagberg N, Weber G, et al. B lymphocytes enhance the interferon-alpha production by plasmacytoid dendritic cells. Arthritis Rheum. 2012;64:3409-19.doi: 10.1002/art.34599doi: 10.1002/art.34599doi: 10.1002/art.34599doi: 10.1002/art.34599doi: 10.1002/art.34599doi: 10.1002/art.34599doi: 10.1002/art.34599doi: 10.1002/art.34599Leonard D, Eloranta ML, Hagberg N, et al. Activated T cells enhance interferon-alpha production by plasmacytoid dendritic cells stimulated with RNA-containing immune complexes. Ann Rheum Dis. 2016;75(9):1728-34. doi: 10.1136/annrheumdis-2015-208055Leonard D, Eloranta ML, Hagberg N, et al. Activated T cells enhance interferon-alpha production by plasmacytoid dendritic cells stimulated with RNA-containing immune complexes. Ann Rheum Dis. 2016;75(9):1728-34. doi: 10.1136/annrheumdis-2015-208055Leonard D, Eloranta ML, Hagberg N, et al. Activated T cells enhance interferon-alpha production by plasmacytoid dendritic cells stimulated with RNA-containing immune complexes. Ann Rheum Dis. 2016;75(9):1728-34. doi: 10.1136/annrheumdis-2015-208055Leonard D, Eloranta ML, Hagberg N, et al. Activated T cells enhance interferon-alpha production by plasmacytoid dendritic cells stimulated with RNA-containing immune complexes. Ann Rheum Dis. 2016;75(9):1728-34. doi: 10.1136/annrheumdis-2015-208055Leonard D, Eloranta ML, Hagberg N, et al. Activated T cells enhance interferon-alpha production by plasmacytoid dendritic cells stimulated with RNA-containing immune complexes. Ann Rheum Dis. 2016;75(9):1728-34. doi: 10.1136/annrheumdis-2015-208055Leonard D, Eloranta ML, Hagberg N, et al. Activated T cells enhance interferon-alpha production by plasmacytoid dendritic cells stimulated with RNA-containing immune complexes. Ann Rheum Dis. 2016;75(9):1728-34. doi: 10.1136/annrheumdis-2015-208055Leonard D, Eloranta ML, Hagberg N, et al. Activated T cells enhance interferon-alpha production by plasmacytoid dendritic cells stimulated with RNA-containing immune complexes. Ann Rheum Dis. 2016;75(9):1728-34. doi: 10.1136/annrheumdis-2015-208055Leonard D, Eloranta ML, Hagberg N, et al. Activated T cells enhance interferon-alpha production by plasmacytoid dendritic cells stimulated with RNA-containing immune complexes. Ann Rheum Dis. 2016;75(9):1728-34. doi: 10.1136/annrheumdis-2015-208055Skurkovich SV, Klinova EG, Eremkina EI, Levina NV. Immunosupressive effect of anti-interferon serum. Nature. 1974;247:551-2. doi: 10.1038/247551a0Skurkovich SV, Klinova EG, Eremkina EI, Levina NV. Immunosupressive effect of anti-interferon serum. Nature. 1974;247:551-2. doi: 10.1038/247551a0Skurkovich SV, Klinova EG, Eremkina EI, Levina NV. Immunosupressive effect of anti-interferon serum. Nature. 1974;247:551-2. doi: 10.1038/247551a0Skurkovich SV, Klinova EG, Eremkina EI, Levina NV. Immunosupressive effect of anti-interferon serum. Nature. 1974;247:551-2. doi: 10.1038/247551a0Skurkovich SV, Klinova EG, Eremkina EI, Levina NV. Immunosupressive effect of anti-interferon serum. Nature. 1974;247:551-2. doi: 10.1038/247551a0Skurkovich SV, Klinova EG, Eremkina EI, Levina NV. Immunosupressive effect of anti-interferon serum. Nature. 1974;247:551-2. doi: 10.1038/247551a0Skurkovich SV, Klinova EG, Eremkina EI, Levina NV. Immunosupressive effect of anti-interferon serum. Nature. 1974;247:551-2. doi: 10.1038/247551a0Skurkovich SV, Klinova EG, Eremkina EI, Levina NV. Immunosupressive effect of anti-interferon serum. Nature. 1974;247:551-2. doi: 10.1038/247551a0Skurkovich SV, Loukina GV, Sigidin YA, Skurkovich BS. Succesful first-time use of antibodies to interferon-gamma alone and combined with antibodies to tumor necrosis factor-alfa to treat rheumatic diseasers (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Behcet`s syndrome). Int J Immunother. 1998;14:23-32.Skurkovich SV, Loukina GV, Sigidin YA, Skurkovich BS. Succesful first-time use of antibodies to interferon-gamma alone and combined with antibodies to tumor necrosis factor-alfa to treat rheumatic diseasers (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Behcet`s syndrome). Int J Immunother. 1998;14:23-32.Skurkovich SV, Loukina GV, Sigidin YA, Skurkovich BS. Succesful first-time use of antibodies to interferon-gamma alone and combined with antibodies to tumor necrosis factor-alfa to treat rheumatic diseasers (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Behcet`s syndrome). Int J Immunother. 1998;14:23-32.Skurkovich SV, Loukina GV, Sigidin YA, Skurkovich BS. Succesful first-time use of antibodies to interferon-gamma alone and combined with antibodies to tumor necrosis factor-alfa to treat rheumatic diseasers (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Behcet`s syndrome). Int J Immunother. 1998;14:23-32.Skurkovich SV, Loukina GV, Sigidin YA, Skurkovich BS. Succesful first-time use of antibodies to interferon-gamma alone and combined with antibodies to tumor necrosis factor-alfa to treat rheumatic diseasers (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Behcet`s syndrome). Int J Immunother. 1998;14:23-32.Skurkovich SV, Loukina GV, Sigidin YA, Skurkovich BS. Succesful first-time use of antibodies to interferon-gamma alone and combined with antibodies to tumor necrosis factor-alfa to treat rheumatic diseasers (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Behcet`s syndrome). Int J Immunother. 1998;14:23-32.Skurkovich SV, Loukina GV, Sigidin YA, Skurkovich BS. Succesful first-time use of antibodies to interferon-gamma alone and combined with antibodies to tumor necrosis factor-alfa to treat rheumatic diseasers (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Behcet`s syndrome). Int J Immunother. 1998;14:23-32.Skurkovich SV, Loukina GV, Sigidin YA, Skurkovich BS. Succesful first-time use of antibodies to interferon-gamma alone and combined with antibodies to tumor necrosis factor-alfa to treat rheumatic diseasers (rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Behcet`s syndrome). Int J Immunother. 1998;14:23-32.Sigidin AY, Loukina GV, Skurkovich B, Skurkovich SV. Randomized double-blind trial of anti-interferob-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol. 2001;30:203-7. doi: 10.1080/030097401316909530Sigidin AY, Loukina GV, Skurkovich B, Skurkovich SV. Randomized double-blind trial of anti-interferob-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol. 2001;30:203-7. doi: 10.1080/030097401316909530Sigidin AY, Loukina GV, Skurkovich B, Skurkovich SV. Randomized double-blind trial of anti-interferob-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol. 2001;30:203-7. doi: 10.1080/030097401316909530Sigidin AY, Loukina GV, Skurkovich B, Skurkovich SV. Randomized double-blind trial of anti-interferob-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol. 2001;30:203-7. doi: 10.1080/030097401316909530Sigidin AY, Loukina GV, Skurkovich B, Skurkovich SV. Randomized double-blind trial of anti-interferob-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol. 2001;30:203-7. doi: 10.1080/030097401316909530Sigidin AY, Loukina GV, Skurkovich B, Skurkovich SV. Randomized double-blind trial of anti-interferob-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol. 2001;30:203-7. doi: 10.1080/030097401316909530Sigidin AY, Loukina GV, Skurkovich B, Skurkovich SV. Randomized double-blind trial of anti-interferob-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol. 2001;30:203-7. doi: 10.1080/030097401316909530Sigidin AY, Loukina GV, Skurkovich B, Skurkovich SV. Randomized double-blind trial of anti-interferob-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol. 2001;30:203-7. doi: 10.1080/030097401316909530Baker KF, Isaacs JD. Novel therapies for immune-mediated inflammatory diseases: What can we learn from their use in rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, psoriasis, Crohn's disease and ulcerative colitis? Ann Rheum Dis. 2018;77(2):175-87. doi: 10.1136/annrheumdis-2017-211555Baker KF, Isaacs JD. Novel therapies for immune-mediated inflammatory diseases: What can we learn from their use in rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, psoriasis, Crohn's disease and ulcerative colitis? Ann Rheum Dis. 2018;77(2):175-87. doi: 10.1136/annrheumdis-2017-211555Baker KF, Isaacs JD. Novel therapies for immune-mediated inflammatory diseases: What can we learn from their use in rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, psoriasis, Crohn's disease and ulcerative colitis? Ann Rheum Dis. 2018;77(2):175-87. doi: 10.1136/annrheumdis-2017-211555Baker KF, Isaacs JD. Novel therapies for immune-mediated inflammatory diseases: What can we learn from their use in rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, psoriasis, Crohn's disease and ulcerative colitis? Ann Rheum Dis. 2018;77(2):175-87. doi: 10.1136/annrheumdis-2017-211555Baker KF, Isaacs JD. Novel therapies for immune-mediated inflammatory diseases: What can we learn from their use in rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, psoriasis, Crohn's disease and ulcerative colitis? Ann Rheum Dis. 2018;77(2):175-87. doi: 10.1136/annrheumdis-2017-211555Baker KF, Isaacs JD. Novel therapies for immune-mediated inflammatory diseases: What can we learn from their use in rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, psoriasis, Crohn's disease and ulcerative colitis? Ann Rheum Dis. 2018;77(2):175-87. doi: 10.1136/annrheumdis-2017-211555Baker KF, Isaacs JD. Novel therapies for immune-mediated inflammatory diseases: What can we learn from their use in rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, psoriasis, Crohn's disease and ulcerative colitis? Ann Rheum Dis. 2018;77(2):175-87. doi: 10.1136/annrheumdis-2017-211555Baker KF, Isaacs JD. Novel therapies for immune-mediated inflammatory diseases: What can we learn from their use in rheumatoid arthritis, spondyloarthritis, systemic lupus erythematosus, psoriasis, Crohn's disease and ulcerative colitis? Ann Rheum Dis. 2018;77(2):175-87. doi: 10.1136/annrheumdis-2017-211555Yao Y, Higgs BW, Morehouse C, et al. Development of potential pharmacodynamic and diagnostic markers for anti-IFN-alpha monoclonal antibody trials in systemic lupus erythematosus. Hum Genom Proteom. 2009:Article ID 374312. doi: 10.4061/2009/37431210.4061/2009/374312Yao Y, Higgs BW, Morehouse C, et al. Development of potential pharmacodynamic and diagnostic markers for anti-IFN-alpha monoclonal antibody trials in systemic lupus erythematosus. Hum Genom Proteom. 2009:Article ID 374312. doi: 10.4061/2009/37431210.4061/2009/374312Yao Y, Higgs BW, Morehouse C, et al. Development of potential pharmacodynamic and diagnostic markers for anti-IFN-alpha monoclonal antibody trials in systemic lupus erythematosus. Hum Genom Proteom. 2009:Article ID 374312. doi: 10.4061/2009/37431210.4061/2009/374312Yao Y, Higgs BW, Morehouse C, et al. Development of potential pharmacodynamic and diagnostic markers for anti-IFN-alpha monoclonal antibody trials in systemic lupus erythematosus. Hum Genom Proteom. 2009:Article ID 374312. doi: 10.4061/2009/37431210.4061/2009/374312Yao Y, Higgs BW, Morehouse C, et al. Development of potential pharmacodynamic and diagnostic markers for anti-IFN-alpha monoclonal antibody trials in systemic lupus erythematosus. Hum Genom Proteom. 2009:Article ID 374312. doi: 10.4061/2009/37431210.4061/2009/374312Yao Y, Higgs BW, Morehouse C, et al. Development of potential pharmacodynamic and diagnostic markers for anti-IFN-alpha monoclonal antibody trials in systemic lupus erythematosus. Hum Genom Proteom. 2009:Article ID 374312. doi: 10.4061/2009/37431210.4061/2009/374312Yao Y, Higgs BW, Morehouse C, et al. Development of potential pharmacodynamic and diagnostic markers for anti-IFN-alpha monoclonal antibody trials in systemic lupus erythematosus. Hum Genom Proteom. 2009:Article ID 374312. doi: 10.4061/2009/37431210.4061/2009/374312Yao Y, Higgs BW, Morehouse C, et al. Development of potential pharmacodynamic and diagnostic markers for anti-IFN-alpha monoclonal antibody trials in systemic lupus erythematosus. Hum Genom Proteom. 2009:Article ID 374312. doi: 10.4061/2009/37431210.4061/2009/374312Merrill JT, Wallace DJ, Petri M, et al. Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis. 2011;70:1905-13. doi: 10.1136/ard.2010.144485Merrill JT, Wallace DJ, Petri M, et al. Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis. 2011;70:1905-13. doi: 10.1136/ard.2010.144485Merrill JT, Wallace DJ, Petri M, et al. Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis. 2011;70:1905-13. doi: 10.1136/ard.2010.144485Merrill JT, Wallace DJ, Petri M, et al. Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis. 2011;70:1905-13. doi: 10.1136/ard.2010.144485Merrill JT, Wallace DJ, Petri M, et al. Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis. 2011;70:1905-13. doi: 10.1136/ard.2010.144485Merrill JT, Wallace DJ, Petri M, et al. Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis. 2011;70:1905-13. doi: 10.1136/ard.2010.144485Merrill JT, Wallace DJ, Petri M, et al. Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis. 2011;70:1905-13. doi: 10.1136/ard.2010.144485Merrill JT, Wallace DJ, Petri M, et al. Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis. 2011;70:1905-13. doi: 10.1136/ard.2010.144485Petri M, Wallace DJ, Spindler A, et al. Sifalimumab, a human anti-interferon-alpha monoclonal antibody, in systemic lupus erythematosus: a phase I randomized, controlled, dose-escalation study. Arthritis Rheum. 2013;65:1011-21. doi: 10.1002/art.37824Petri M, Wallace DJ, Spindler A, et al. Sifalimumab, a human anti-interferon-alpha monoclonal antibody, in systemic lupus erythematosus: a phase I randomized, controlled, dose-escalation study. Arthritis Rheum. 2013;65:1011-21. doi: 10.1002/art.37824Petri M, Wallace DJ, Spindler A, et al. Sifalimumab, a human anti-interferon-alpha monoclonal antibody, in systemic lupus erythematosus: a phase I randomized, controlled, dose-escalation study. Arthritis Rheum. 2013;65:1011-21. doi: 10.1002/art.37824Petri M, Wallace DJ, Spindler A, et al. Sifalimumab, a human anti-interferon-alpha monoclonal antibody, in systemic lupus erythematosus: a phase I randomized, controlled, dose-escalation study. Arthritis Rheum. 2013;65:1011-21. doi: 10.1002/art.37824Petri M, Wallace DJ, Spindler A, et al. Sifalimumab, a human anti-interferon-alpha monoclonal antibody, in systemic lupus erythematosus: a phase I randomized, controlled, dose-escalation study. Arthritis Rheum. 2013;65:1011-21. doi: 10.1002/art.37824Petri M, Wallace DJ, Spindler A, et al. Sifalimumab, a human anti-interferon-alpha monoclonal antibody, in systemic lupus erythematosus: a phase I randomized, controlled, dose-escalation study. Arthritis Rheum. 2013;65:1011-21. doi: 10.1002/art.37824Petri M, Wallace DJ, Spindler A, et al. Sifalimumab, a human anti-interferon-alpha monoclonal antibody, in systemic lupus erythematosus: a phase I randomized, controlled, dose-escalation study. Arthritis Rheum. 2013;65:1011-21. doi: 10.1002/art.37824Petri M, Wallace DJ, Spindler A, et al. Sifalimumab, a human anti-interferon-alpha monoclonal antibody, in systemic lupus erythematosus: a phase I randomized, controlled, dose-escalation study. Arthritis Rheum. 2013;65:1011-21. doi: 10.1002/art.37824Khamashta M, Merrill JT, Werth VP, et al. Sifalimumab, an antiinterferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909-16. doi: 10.1136/annrheumdis-2015-208562Khamashta M, Merrill JT, Werth VP, et al. Sifalimumab, an antiinterferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909-16. doi: 10.1136/annrheumdis-2015-208562Khamashta M, Merrill JT, Werth VP, et al. Sifalimumab, an antiinterferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909-16. doi: 10.1136/annrheumdis-2015-208562Khamashta M, Merrill JT, Werth VP, et al. Sifalimumab, an antiinterferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909-16. doi: 10.1136/annrheumdis-2015-208562Khamashta M, Merrill JT, Werth VP, et al. Sifalimumab, an antiinterferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909-16. doi: 10.1136/annrheumdis-2015-208562Khamashta M, Merrill JT, Werth VP, et al. Sifalimumab, an antiinterferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909-16. doi: 10.1136/annrheumdis-2015-208562Khamashta M, Merrill JT, Werth VP, et al. Sifalimumab, an antiinterferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909-16. doi: 10.1136/annrheumdis-2015-208562Khamashta M, Merrill JT, Werth VP, et al. Sifalimumab, an antiinterferon-α monoclonal antibody, in moderate to severe systemic lupus erythematosus: a randomised, double-blind, placebo-controlled study. Ann Rheum Dis. 2016;75:1909-16. doi: 10.1136/annrheumdis-2015-208562Tcherepanova I, Curtis M, Sale M, et al. SAT0193 Results of a randomized placebo controlled phase ia study of AGS-009, a humanized anti-interferon-α monoclonal antibody in subjects with systemic lupus erythematosus. Ann Rheum Dis. 2013;71(Suppl 3):536.3-7. doi: 10.1136/annrheumdis-2012-eular.3140Tcherepanova I, Curtis M, Sale M, et al. SAT0193 Results of a randomized placebo controlled phase ia study of AGS-009, a humanized anti-interferon-α monoclonal antibody in subjects with systemic lupus erythematosus. Ann Rheum Dis. 2013;71(Suppl 3):536.3-7. doi: 10.1136/annrheumdis-2012-eular.3140Tcherepanova I, Curtis M, Sale M, et al. SAT0193 Results of a randomized placebo controlled phase ia study of AGS-009, a humanized anti-interferon-α monoclonal antibody in subjects with systemic lupus erythematosus. Ann Rheum Dis. 2013;71(Suppl 3):536.3-7. doi: 10.1136/annrheumdis-2012-eular.3140Tcherepanova I, Curtis M, Sale M, et al. SAT0193 Results of a randomized placebo controlled phase ia study of AGS-009, a humanized anti-interferon-α monoclonal antibody in subjects with systemic lupus erythematosus. Ann Rheum Dis. 2013;71(Suppl 3):536.3-7. doi: 10.1136/annrheumdis-2012-eular.3140Tcherepanova I, Curtis M, Sale M, et al. SAT0193 Results of a randomized placebo controlled phase ia study of AGS-009, a humanized anti-interferon-α monoclonal antibody in subjects with systemic lupus erythematosus. Ann Rheum Dis. 2013;71(Suppl 3):536.3-7. doi: 10.1136/annrheumdis-2012-eular.3140Tcherepanova I, Curtis M, Sale M, et al. SAT0193 Results of a randomized placebo controlled phase ia study of AGS-009, a humanized anti-interferon-α monoclonal antibody in subjects with systemic lupus erythematosus. Ann Rheum Dis. 2013;71(Suppl 3):536.3-7. doi: 10.1136/annrheumdis-2012-eular.3140Tcherepanova I, Curtis M, Sale M, et al. SAT0193 Results of a randomized placebo controlled phase ia study of AGS-009, a humanized anti-interferon-α monoclonal antibody in subjects with systemic lupus erythematosus. Ann Rheum Dis. 2013;71(Suppl 3):536.3-7. doi: 10.1136/annrheumdis-2012-eular.3140Tcherepanova I, Curtis M, Sale M, et al. SAT0193 Results of a randomized placebo controlled phase ia study of AGS-009, a humanized anti-interferon-α monoclonal antibody in subjects with systemic lupus erythematosus. Ann Rheum Dis. 2013;71(Suppl 3):536.3-7. doi: 10.1136/annrheumdis-2012-eular.3140Kalunian KC, Merrill JT, Maciuca R, et al. A phase II study of the efficacy and safety of rontalizumab (rhuMAb interferon-α) in patients with systemic lupus erythematosus (ROSE). Ann Rheum Dis. 2016;75:196-202. doi: 10.1136/annrheumdis-2014-206090Kalunian KC, Merrill JT, Maciuca R, et al. A phase II study of the efficacy and safety of rontalizumab (rhuMAb interferon-α) in patients with systemic lupus erythematosus (ROSE). Ann Rheum Dis. 2016;75:196-202. doi: 10.1136/annrheumdis-2014-206090Kalunian KC, Merrill JT, Maciuca R, et al. A phase II study of the efficacy and safety of rontalizumab (rhuMAb interferon-α) in patients with systemic lupus erythematosus (ROSE). Ann Rheum Dis. 2016;75:196-202. doi: 10.1136/annrheumdis-2014-206090Kalunian KC, Merrill JT, Maciuca R, et al. A phase II study of the efficacy and safety of rontalizumab (rhuMAb interferon-α) in patients with systemic lupus erythematosus (ROSE). Ann Rheum Dis. 2016;75:196-202. doi: 10.1136/annrheumdis-2014-206090Kalunian KC, Merrill JT, Maciuca R, et al. A phase II study of the efficacy and safety of rontalizumab (rhuMAb interferon-α) in patients with systemic lupus erythematosus (ROSE). Ann Rheum Dis. 2016;75:196-202. doi: 10.1136/annrheumdis-2014-206090Kalunian KC, Merrill JT, Maciuca R, et al. A phase II study of the efficacy and safety of rontalizumab (rhuMAb interferon-α) in patients with systemic lupus erythematosus (ROSE). Ann Rheum Dis. 2016;75:196-202. doi: 10.1136/annrheumdis-2014-206090Kalunian KC, Merrill JT, Maciuca R, et al. A phase II study of the efficacy and safety of rontalizumab (rhuMAb interferon-α) in patients with systemic lupus erythematosus (ROSE). Ann Rheum Dis. 2016;75:196-202. doi: 10.1136/annrheumdis-2014-206090Kalunian KC, Merrill JT, Maciuca R, et al. A phase II study of the efficacy and safety of rontalizumab (rhuMAb interferon-α) in patients with systemic lupus erythematosus (ROSE). Ann Rheum Dis. 2016;75:196-202. doi: 10.1136/annrheumdis-2014-206090Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7:428-39. doi: 10.1080/19420862.2015.1007810Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7:428-39. doi: 10.1080/19420862.2015.1007810Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7:428-39. doi: 10.1080/19420862.2015.1007810Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7:428-39. doi: 10.1080/19420862.2015.1007810Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7:428-39. doi: 10.1080/19420862.2015.1007810Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7:428-39. doi: 10.1080/19420862.2015.1007810Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7:428-39. doi: 10.1080/19420862.2015.1007810Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7:428-39. doi: 10.1080/19420862.2015.1007810Riggs JM, Hanna RN, Rajan B, et al. Characterisation of anifrolumab, a fully human anti-interferon receptor antagonist antibody for the treatment of systemic lupus erythematosus. Lupus Sci Med. 2018;5:e000261. doi: 10.1136/lupus-2018-000261Riggs JM, Hanna RN, Rajan B, et al. Characterisation of anifrolumab, a fully human anti-interferon receptor antagonist antibody for the treatment of systemic lupus erythematosus. Lupus Sci Med. 2018;5:e000261. doi: 10.1136/lupus-2018-000261Riggs JM, Hanna RN, Rajan B, et al. Characterisation of anifrolumab, a fully human anti-interferon receptor antagonist antibody for the treatment of systemic lupus erythematosus. Lupus Sci Med. 2018;5:e000261. doi: 10.1136/lupus-2018-000261Riggs JM, Hanna RN, Rajan B, et al. Characterisation of anifrolumab, a fully human anti-interferon receptor antagonist antibody for the treatment of systemic lupus erythematosus. Lupus Sci Med. 2018;5:e000261. doi: 10.1136/lupus-2018-000261Riggs JM, Hanna RN, Rajan B, et al. Characterisation of anifrolumab, a fully human anti-interferon receptor antagonist antibody for the treatment of systemic lupus erythematosus. Lupus Sci Med. 2018;5:e000261. doi: 10.1136/lupus-2018-000261Riggs JM, Hanna RN, Rajan B, et al. Characterisation of anifrolumab, a fully human anti-interferon receptor antagonist antibody for the treatment of systemic lupus erythematosus. Lupus Sci Med. 2018;5:e000261. doi: 10.1136/lupus-2018-000261Riggs JM, Hanna RN, Rajan B, et al. Characterisation of anifrolumab, a fully human anti-interferon receptor antagonist antibody for the treatment of systemic lupus erythematosus. Lupus Sci Med. 2018;5:e000261. doi: 10.1136/lupus-2018-000261Riggs JM, Hanna RN, Rajan B, et al. Characterisation of anifrolumab, a fully human anti-interferon receptor antagonist antibody for the treatment of systemic lupus erythematosus. Lupus Sci Med. 2018;5:e000261. doi: 10.1136/lupus-2018-000261Felten R, Scher F, Sagez F, et al. Spotlight on anifrolumab and its potential for the treatment of moderate-to-severe systemic lupus erythematosus: evidence to date. Drug Des Devel Ther. 2019;13:1535-43. doi: 10.2147/DDDT.S170969Felten R, Scher F, Sagez F, et al. Spotlight on anifrolumab and its potential for the treatment of moderate-to-severe systemic lupus erythematosus: evidence to date. Drug Des Devel Ther. 2019;13:1535-43. doi: 10.2147/DDDT.S170969Felten R, Scher F, Sagez F, et al. Spotlight on anifrolumab and its potential for the treatment of moderate-to-severe systemic lupus erythematosus: evidence to date. Drug Des Devel Ther. 2019;13:1535-43. doi: 10.2147/DDDT.S170969Felten R, Scher F, Sagez F, et al. Spotlight on anifrolumab and its potential for the treatment of moderate-to-severe systemic lupus erythematosus: evidence to date. Drug Des Devel Ther. 2019;13:1535-43. doi: 10.2147/DDDT.S170969Felten R, Scher F, Sagez F, et al. Spotlight on anifrolumab and its potential for the treatment of moderate-to-severe systemic lupus erythematosus: evidence to date. Drug Des Devel Ther. 2019;13:1535-43. doi: 10.2147/DDDT.S170969Felten R, Scher F, Sagez F, et al. Spotlight on anifrolumab and its potential for the treatment of moderate-to-severe systemic lupus erythematosus: evidence to date. Drug Des Devel Ther. 2019;13:1535-43. doi: 10.2147/DDDT.S170969Felten R, Scher F, Sagez F, et al. Spotlight on anifrolumab and its potential for the treatment of moderate-to-severe systemic lupus erythematosus: evidence to date. Drug Des Devel Ther. 2019;13:1535-43. doi: 10.2147/DDDT.S170969Felten R, Scher F, Sagez F, et al. Spotlight on anifrolumab and its potential for the treatment of moderate-to-severe systemic lupus erythematosus: evidence to date. Drug Des Devel Ther. 2019;13:1535-43. doi: 10.2147/DDDT.S170969Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an antiinterferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheum. 2017;69:376-86. doi: 10.1002/art.39962Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an antiinterferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheum. 2017;69:376-86. doi: 10.1002/art.39962Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an antiinterferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheum. 2017;69:376-86. doi: 10.1002/art.39962Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an antiinterferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheum. 2017;69:376-86. doi: 10.1002/art.39962Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an antiinterferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheum. 2017;69:376-86. doi: 10.1002/art.39962Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an antiinterferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheum. 2017;69:376-86. doi: 10.1002/art.39962Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an antiinterferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheum. 2017;69:376-86. doi: 10.1002/art.39962Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an antiinterferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus. Arthritis Rheum. 2017;69:376-86. doi: 10.1002/art.39962Merrill JT, Furie R, Werth VP, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med. 2018;5(1):e000284. doi: 10.1136/lupus-2018-000284Merrill JT, Furie R, Werth VP, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med. 2018;5(1):e000284. doi: 10.1136/lupus-2018-000284Merrill JT, Furie R, Werth VP, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med. 2018;5(1):e000284. doi: 10.1136/lupus-2018-000284Merrill JT, Furie R, Werth VP, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med. 2018;5(1):e000284. doi: 10.1136/lupus-2018-000284Merrill JT, Furie R, Werth VP, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med. 2018;5(1):e000284. doi: 10.1136/lupus-2018-000284Merrill JT, Furie R, Werth VP, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med. 2018;5(1):e000284. doi: 10.1136/lupus-2018-000284Merrill JT, Furie R, Werth VP, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med. 2018;5(1):e000284. doi: 10.1136/lupus-2018-000284Merrill JT, Furie R, Werth VP, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med. 2018;5(1):e000284. doi: 10.1136/lupus-2018-000284Casey KA, Guo X, Smith MA, et al. Type I interferon receptor blockade with anifrolumab corrects innate and adaptive immune perturbations of SLE. Lupus Sci Med. 2018;5(1):e000286. doi: 10.1136/lupus-2018-000286Casey KA, Guo X, Smith MA, et al. Type I interferon receptor blockade with anifrolumab corrects innate and adaptive immune perturbations of SLE. Lupus Sci Med. 2018;5(1):e000286. doi: 10.1136/lupus-2018-000286Casey KA, Guo X, Smith MA, et al. Type I interferon receptor blockade with anifrolumab corrects innate and adaptive immune perturbations of SLE. Lupus Sci Med. 2018;5(1):e000286. doi: 10.1136/lupus-2018-000286Casey KA, Guo X, Smith MA, et al. Type I interferon receptor blockade with anifrolumab corrects innate and adaptive immune perturbations of SLE. Lupus Sci Med. 2018;5(1):e000286. doi: 10.1136/lupus-2018-000286Casey KA, Guo X, Smith MA, et al. Type I interferon receptor blockade with anifrolumab corrects innate and adaptive immune perturbations of SLE. Lupus Sci Med. 2018;5(1):e000286. doi: 10.1136/lupus-2018-000286Casey KA, Guo X, Smith MA, et al. Type I interferon receptor blockade with anifrolumab corrects innate and adaptive immune perturbations of SLE. Lupus Sci Med. 2018;5(1):e000286. doi: 10.1136/lupus-2018-000286Casey KA, Guo X, Smith MA, et al. Type I interferon receptor blockade with anifrolumab corrects innate and adaptive immune perturbations of SLE. Lupus Sci Med. 2018;5(1):e000286. doi: 10.1136/lupus-2018-000286Casey KA, Guo X, Smith MA, et al. Type I interferon receptor blockade with anifrolumab corrects innate and adaptive immune perturbations of SLE. Lupus Sci Med. 2018;5(1):e000286. doi: 10.1136/lupus-2018-000286Goldberg A, Geppert T, Schiopu E, et al. Dose-escalation of human anti-interferon-α receptor monoclonal antibody MEDI-546 in subjects with systemic sclerosis: a phase 1, multicenter, open label study. Arthritis Res Ther. 2014;16:R57.Goldberg A, Geppert T, Schiopu E, et al. Dose-escalation of human anti-interferon-α receptor monoclonal antibody MEDI-546 in subjects with systemic sclerosis: a phase 1, multicenter, open label study. Arthritis Res Ther. 2014;16:R57.Goldberg A, Geppert T, Schiopu E, et al. Dose-escalation of human anti-interferon-α receptor monoclonal antibody MEDI-546 in subjects with systemic sclerosis: a phase 1, multicenter, open label study. Arthritis Res Ther. 2014;16:R57.Goldberg A, Geppert T, Schiopu E, et al. Dose-escalation of human anti-interferon-α receptor monoclonal antibody MEDI-546 in subjects with systemic sclerosis: a phase 1, multicenter, open label study. Arthritis Res Ther. 2014;16:R57.Goldberg A, Geppert T, Schiopu E, et al. Dose-escalation of human anti-interferon-α receptor monoclonal antibody MEDI-546 in subjects with systemic sclerosis: a phase 1, multicenter, open label study. Arthritis Res Ther. 2014;16:R57.Goldberg A, Geppert T, Schiopu E, et al. Dose-escalation of human anti-interferon-α receptor monoclonal antibody MEDI-546 in subjects with systemic sclerosis: a phase 1, multicenter, open label study. Arthritis Res Ther. 2014;16:R57.Goldberg A, Geppert T, Schiopu E, et al. Dose-escalation of human anti-interferon-α receptor monoclonal antibody MEDI-546 in subjects with systemic sclerosis: a phase 1, multicenter, open label study. Arthritis Res Ther. 2014;16:R57.Goldberg A, Geppert T, Schiopu E, et al. Dose-escalation of human anti-interferon-α receptor monoclonal antibody MEDI-546 in subjects with systemic sclerosis: a phase 1, multicenter, open label study. Arthritis Res Ther. 2014;16:R57.doi: 10.1186/ar4492doi: 10.1186/ar4492doi: 10.1186/ar4492doi: 10.1186/ar4492doi: 10.1186/ar4492doi: 10.1186/ar4492doi: 10.1186/ar4492doi: 10.1186/ar4492Update on TULIP 1 phase III trial for anifrolumab in systemic lupus erythematosus. Available from: https://www.astrazeneca.com/media-centre/press-releases/2018/update-on-tulip-1-phase-iii-trial-for-anifrolumab-insystemic-lupus-erythematosus-31082018.html. Accessed January 10, 2019.Update on TULIP 1 phase III trial for anifrolumab in systemic lupus erythematosus. Available from: https://www.astrazeneca.com/media-centre/press-releases/2018/update-on-tulip-1-phase-iii-trial-for-anifrolumab-insystemic-lupus-erythematosus-31082018.html. Accessed January 10, 2019.Update on TULIP 1 phase III trial for anifrolumab in systemic lupus erythematosus. Available from: https://www.astrazeneca.com/media-centre/press-releases/2018/update-on-tulip-1-phase-iii-trial-for-anifrolumab-insystemic-lupus-erythematosus-31082018.html. Accessed January 10, 2019.Update on TULIP 1 phase III trial for anifrolumab in systemic lupus erythematosus. Available from: https://www.astrazeneca.com/media-centre/press-releases/2018/update-on-tulip-1-phase-iii-trial-for-anifrolumab-insystemic-lupus-erythematosus-31082018.html. Accessed January 10, 2019.Update on TULIP 1 phase III trial for anifrolumab in systemic lupus erythematosus. Available from: https://www.astrazeneca.com/media-centre/press-releases/2018/update-on-tulip-1-phase-iii-trial-for-anifrolumab-insystemic-lupus-erythematosus-31082018.html. Accessed January 10, 2019.Update on TULIP 1 phase III trial for anifrolumab in systemic lupus erythematosus. Available from: https://www.astrazeneca.com/media-centre/press-releases/2018/update-on-tulip-1-phase-iii-trial-for-anifrolumab-insystemic-lupus-erythematosus-31082018.html. Accessed January 10, 2019.Update on TULIP 1 phase III trial for anifrolumab in systemic lupus erythematosus. Available from: https://www.astrazeneca.com/media-centre/press-releases/2018/update-on-tulip-1-phase-iii-trial-for-anifrolumab-insystemic-lupus-erythematosus-31082018.html. Accessed January 10, 2019.Update on TULIP 1 phase III trial for anifrolumab in systemic lupus erythematosus. Available from: https://www.astrazeneca.com/media-centre/press-releases/2018/update-on-tulip-1-phase-iii-trial-for-anifrolumab-insystemic-lupus-erythematosus-31082018.html. Accessed January 10, 2019.Schwartz DM, Kanno Y, Villarino A, et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-62. doi: 10.1038/nrd.2017.201Schwartz DM, Kanno Y, Villarino A, et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-62. doi: 10.1038/nrd.2017.201Schwartz DM, Kanno Y, Villarino A, et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-62. doi: 10.1038/nrd.2017.201Schwartz DM, Kanno Y, Villarino A, et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-62. doi: 10.1038/nrd.2017.201Schwartz DM, Kanno Y, Villarino A, et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-62. doi: 10.1038/nrd.2017.201Schwartz DM, Kanno Y, Villarino A, et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-62. doi: 10.1038/nrd.2017.201Schwartz DM, Kanno Y, Villarino A, et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-62. doi: 10.1038/nrd.2017.201Schwartz DM, Kanno Y, Villarino A, et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-62. doi: 10.1038/nrd.2017.201Nasonov EL, Lila AM. Janus kinase inhibitors in immuno-inflammatory rheumatic diseases: new opportunities and prospects. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2019;57(1):8-16 (In Russ.). doi: 10.14412/1995-4484-2019-8-16Nasonov EL, Lila AM. Janus kinase inhibitors in immuno-inflammatory rheumatic diseases: new opportunities and prospects. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2019;57(1):8-16 (In Russ.). doi: 10.14412/1995-4484-2019-8-16Nasonov EL, Lila AM. Janus kinase inhibitors in immuno-inflammatory rheumatic diseases: new opportunities and prospects. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2019;57(1):8-16 (In Russ.). doi: 10.14412/1995-4484-2019-8-16Nasonov EL, Lila AM. Janus kinase inhibitors in immuno-inflammatory rheumatic diseases: new opportunities and prospects. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2019;57(1):8-16 (In Russ.). doi: 10.14412/1995-4484-2019-8-16Nasonov EL, Lila AM. Janus kinase inhibitors in immuno-inflammatory rheumatic diseases: new opportunities and prospects. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2019;57(1):8-16 (In Russ.). doi: 10.14412/1995-4484-2019-8-16Nasonov EL, Lila AM. Janus kinase inhibitors in immuno-inflammatory rheumatic diseases: new opportunities and prospects. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2019;57(1):8-16 (In Russ.). doi: 10.14412/1995-4484-2019-8-16Nasonov EL, Lila AM. Janus kinase inhibitors in immuno-inflammatory rheumatic diseases: new opportunities and prospects. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2019;57(1):8-16 (In Russ.). doi: 10.14412/1995-4484-2019-8-16Nasonov EL, Lila AM. Janus kinase inhibitors in immuno-inflammatory rheumatic diseases: new opportunities and prospects. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2019;57(1):8-16 (In Russ.). doi: 10.14412/1995-4484-2019-8-16Mok CC. The Jakinibs in systemic lupus erythematosus: progress and prospects. Expert Opin Investig Drugs. 2019;28(1):85-92. doi: 10.1080/13543784.2019.1551358Mok CC. The Jakinibs in systemic lupus erythematosus: progress and prospects. Expert Opin Investig Drugs. 2019;28(1):85-92. doi: 10.1080/13543784.2019.1551358Mok CC. The Jakinibs in systemic lupus erythematosus: progress and prospects. Expert Opin Investig Drugs. 2019;28(1):85-92. doi: 10.1080/13543784.2019.1551358Mok CC. The Jakinibs in systemic lupus erythematosus: progress and prospects. Expert Opin Investig Drugs. 2019;28(1):85-92. doi: 10.1080/13543784.2019.1551358Mok CC. The Jakinibs in systemic lupus erythematosus: progress and prospects. Expert Opin Investig Drugs. 2019;28(1):85-92. doi: 10.1080/13543784.2019.1551358Mok CC. The Jakinibs in systemic lupus erythematosus: progress and prospects. Expert Opin Investig Drugs. 2019;28(1):85-92. doi: 10.1080/13543784.2019.1551358Mok CC. The Jakinibs in systemic lupus erythematosus: progress and prospects. Expert Opin Investig Drugs. 2019;28(1):85-92. doi: 10.1080/13543784.2019.1551358Mok CC. The Jakinibs in systemic lupus erythematosus: progress and prospects. Expert Opin Investig Drugs. 2019;28(1):85-92. doi: 10.1080/13543784.2019.1551358Sanchez GAM, Reinhardt A, Ramsey S, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;128(7):3041-52. doi: 10.1172/JCI98814Sanchez GAM, Reinhardt A, Ramsey S, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;128(7):3041-52. doi: 10.1172/JCI98814Sanchez GAM, Reinhardt A, Ramsey S, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;128(7):3041-52. doi: 10.1172/JCI98814Sanchez GAM, Reinhardt A, Ramsey S, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;128(7):3041-52. doi: 10.1172/JCI98814Sanchez GAM, Reinhardt A, Ramsey S, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;128(7):3041-52. doi: 10.1172/JCI98814Sanchez GAM, Reinhardt A, Ramsey S, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;128(7):3041-52. doi: 10.1172/JCI98814Sanchez GAM, Reinhardt A, Ramsey S, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;128(7):3041-52. doi: 10.1172/JCI98814Sanchez GAM, Reinhardt A, Ramsey S, et al. JAK1/2 inhibition with baricitinib in the treatment of autoinflammatory interferonopathies. J Clin Invest. 2018;128(7):3041-52. doi: 10.1172/JCI98814Kö nig N, Fiehn C, Wolf C, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2017;76(2):468-72.Kö nig N, Fiehn C, Wolf C, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2017;76(2):468-72.Kö nig N, Fiehn C, Wolf C, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2017;76(2):468-72.Kö nig N, Fiehn C, Wolf C, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2017;76(2):468-72.Kö nig N, Fiehn C, Wolf C, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2017;76(2):468-72.Kö nig N, Fiehn C, Wolf C, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2017;76(2):468-72.Kö nig N, Fiehn C, Wolf C, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2017;76(2):468-72.Kö nig N, Fiehn C, Wolf C, et al. Familial chilblain lupus due to a gain-of-function mutation in STING. Ann Rheum Dis. 2017;76(2):468-72.Rodero MP, Fremond M-L, Rice GI, et al. JAK inhibition in STING-associated interferonopathy. Ann Rheum Dis. 2016;75(12):e75. doi: 10.1136/annrheumdis-2016-210504Rodero MP, Fremond M-L, Rice GI, et al. JAK inhibition in STING-associated interferonopathy. Ann Rheum Dis. 2016;75(12):e75. doi: 10.1136/annrheumdis-2016-210504Rodero MP, Fremond M-L, Rice GI, et al. JAK inhibition in STING-associated interferonopathy. Ann Rheum Dis. 2016;75(12):e75. doi: 10.1136/annrheumdis-2016-210504Rodero MP, Fremond M-L, Rice GI, et al. JAK inhibition in STING-associated interferonopathy. Ann Rheum Dis. 2016;75(12):e75. doi: 10.1136/annrheumdis-2016-210504Rodero MP, Fremond M-L, Rice GI, et al. JAK inhibition in STING-associated interferonopathy. Ann Rheum Dis. 2016;75(12):e75. doi: 10.1136/annrheumdis-2016-210504Rodero MP, Fremond M-L, Rice GI, et al. JAK inhibition in STING-associated interferonopathy. Ann Rheum Dis. 2016;75(12):e75. doi: 10.1136/annrheumdis-2016-210504Rodero MP, Fremond M-L, Rice GI, et al. JAK inhibition in STING-associated interferonopathy. Ann Rheum Dis. 2016;75(12):e75. doi: 10.1136/annrheumdis-2016-210504Rodero MP, Fremond M-L, Rice GI, et al. JAK inhibition in STING-associated interferonopathy. Ann Rheum Dis. 2016;75(12):e75. doi: 10.1136/annrheumdis-2016-210504Seo J, Kang J-A, Suh DI, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139(4):1396-9.e12. doi: 10.1016/j.jaci.2016.10.030Seo J, Kang J-A, Suh DI, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139(4):1396-9.e12. doi: 10.1016/j.jaci.2016.10.030Seo J, Kang J-A, Suh DI, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139(4):1396-9.e12. doi: 10.1016/j.jaci.2016.10.030Seo J, Kang J-A, Suh DI, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139(4):1396-9.e12. doi: 10.1016/j.jaci.2016.10.030Seo J, Kang J-A, Suh DI, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139(4):1396-9.e12. doi: 10.1016/j.jaci.2016.10.030Seo J, Kang J-A, Suh DI, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139(4):1396-9.e12. doi: 10.1016/j.jaci.2016.10.030Seo J, Kang J-A, Suh DI, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139(4):1396-9.e12. doi: 10.1016/j.jaci.2016.10.030Seo J, Kang J-A, Suh DI, et al. Tofacitinib relieves symptoms of stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy caused by 2 de novo variants in TMEM173. J Allergy Clin Immunol. 2017;139(4):1396-9.e12. doi: 10.1016/j.jaci.2016.10.030Volpi S, Insalaco A, Caorsi R, et al. Efficacy and Adverse Events During Janus Kinase Inhibitor Treatment of SAVI Syndrome. J Clin Immunol. 2019 Jul;39(5):476-85. doi: 10.1007/s10875-019-00645-0Volpi S, Insalaco A, Caorsi R, et al. Efficacy and Adverse Events During Janus Kinase Inhibitor Treatment of SAVI Syndrome. J Clin Immunol. 2019 Jul;39(5):476-85. doi: 10.1007/s10875-019-00645-0Volpi S, Insalaco A, Caorsi R, et al. Efficacy and Adverse Events During Janus Kinase Inhibitor Treatment of SAVI Syndrome. J Clin Immunol. 2019 Jul;39(5):476-85. doi: 10.1007/s10875-019-00645-0Volpi S, Insalaco A, Caorsi R, et al. Efficacy and Adverse Events During Janus Kinase Inhibitor Treatment of SAVI Syndrome. J Clin Immunol. 2019 Jul;39(5):476-85. doi: 10.1007/s10875-019-00645-0Volpi S, Insalaco A, Caorsi R, et al. Efficacy and Adverse Events During Janus Kinase Inhibitor Treatment of SAVI Syndrome. J Clin Immunol. 2019 Jul;39(5):476-85. doi: 10.1007/s10875-019-00645-0Volpi S, Insalaco A, Caorsi R, et al. Efficacy and Adverse Events During Janus Kinase Inhibitor Treatment of SAVI Syndrome. J Clin Immunol. 2019 Jul;39(5):476-85. doi: 10.1007/s10875-019-00645-0Volpi S, Insalaco A, Caorsi R, et al. Efficacy and Adverse Events During Janus Kinase Inhibitor Treatment of SAVI Syndrome. J Clin Immunol. 2019 Jul;39(5):476-85. doi: 10.1007/s10875-019-00645-0Volpi S, Insalaco A, Caorsi R, et al. Efficacy and Adverse Events During Janus Kinase Inhibitor Treatment of SAVI Syndrome. J Clin Immunol. 2019 Jul;39(5):476-85. doi: 10.1007/s10875-019-00645-0Ikeda K, Hayakawa K, Fujishiro M, et al. JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation. BMC Immunol. 2017;18(1):41. doi: 10.1186/s12865-017-0225-9Ikeda K, Hayakawa K, Fujishiro M, et al. JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation. BMC Immunol. 2017;18(1):41. doi: 10.1186/s12865-017-0225-9Ikeda K, Hayakawa K, Fujishiro M, et al. JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation. BMC Immunol. 2017;18(1):41. doi: 10.1186/s12865-017-0225-9Ikeda K, Hayakawa K, Fujishiro M, et al. JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation. BMC Immunol. 2017;18(1):41. doi: 10.1186/s12865-017-0225-9Ikeda K, Hayakawa K, Fujishiro M, et al. JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation. BMC Immunol. 2017;18(1):41. doi: 10.1186/s12865-017-0225-9Ikeda K, Hayakawa K, Fujishiro M, et al. JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation. BMC Immunol. 2017;18(1):41. doi: 10.1186/s12865-017-0225-9Ikeda K, Hayakawa K, Fujishiro M, et al. JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation. BMC Immunol. 2017;18(1):41. doi: 10.1186/s12865-017-0225-9Ikeda K, Hayakawa K, Fujishiro M, et al. JAK inhibitor has the amelioration effect in lupus-prone mice: the involvement of IFN signature gene downregulation. BMC Immunol. 2017;18(1):41. doi: 10.1186/s12865-017-0225-9Furumoto Y, Smith CK, Blanco L, et al. Tofacitinib Ameliorates Murine Lupus and Its Associated Vascular Dysfunction. Arthritis Rheum. 2017;69(1):148-60. doi: 10.1002/art.39818Furumoto Y, Smith CK, Blanco L, et al. Tofacitinib Ameliorates Murine Lupus and Its Associated Vascular Dysfunction. Arthritis Rheum. 2017;69(1):148-60. doi: 10.1002/art.39818Furumoto Y, Smith CK, Blanco L, et al. Tofacitinib Ameliorates Murine Lupus and Its Associated Vascular Dysfunction. Arthritis Rheum. 2017;69(1):148-60. doi: 10.1002/art.39818Furumoto Y, Smith CK, Blanco L, et al. Tofacitinib Ameliorates Murine Lupus and Its Associated Vascular Dysfunction. Arthritis Rheum. 2017;69(1):148-60. doi: 10.1002/art.39818Furumoto Y, Smith CK, Blanco L, et al. Tofacitinib Ameliorates Murine Lupus and Its Associated Vascular Dysfunction. Arthritis Rheum. 2017;69(1):148-60. doi: 10.1002/art.39818Furumoto Y, Smith CK, Blanco L, et al. Tofacitinib Ameliorates Murine Lupus and Its Associated Vascular Dysfunction. Arthritis Rheum. 2017;69(1):148-60. doi: 10.1002/art.39818Furumoto Y, Smith CK, Blanco L, et al. Tofacitinib Ameliorates Murine Lupus and Its Associated Vascular Dysfunction. Arthritis Rheum. 2017;69(1):148-60. doi: 10.1002/art.39818Furumoto Y, Smith CK, Blanco L, et al. Tofacitinib Ameliorates Murine Lupus and Its Associated Vascular Dysfunction. Arthritis Rheum. 2017;69(1):148-60. doi: 10.1002/art.39818Yamamoto M, Yokoyama Y, Shimizu Y, et al. Tofacitinib can decrease anti-DNA antibody titers in inactive systemic lupus erythematosus complicated by rheumatoid arthritis. Mod Rheumatol. 2016;26(4):633-4. doi: 10.3109/14397595.2015.1069473Yamamoto M, Yokoyama Y, Shimizu Y, et al. Tofacitinib can decrease anti-DNA antibody titers in inactive systemic lupus erythematosus complicated by rheumatoid arthritis. Mod Rheumatol. 2016;26(4):633-4. doi: 10.3109/14397595.2015.1069473Yamamoto M, Yokoyama Y, Shimizu Y, et al. Tofacitinib can decrease anti-DNA antibody titers in inactive systemic lupus erythematosus complicated by rheumatoid arthritis. Mod Rheumatol. 2016;26(4):633-4. doi: 10.3109/14397595.2015.1069473Yamamoto M, Yokoyama Y, Shimizu Y, et al. Tofacitinib can decrease anti-DNA antibody titers in inactive systemic lupus erythematosus complicated by rheumatoid arthritis. Mod Rheumatol. 2016;26(4):633-4. doi: 10.3109/14397595.2015.1069473Yamamoto M, Yokoyama Y, Shimizu Y, et al. Tofacitinib can decrease anti-DNA antibody titers in inactive systemic lupus erythematosus complicated by rheumatoid arthritis. Mod Rheumatol. 2016;26(4):633-4. doi: 10.3109/14397595.2015.1069473Yamamoto M, Yokoyama Y, Shimizu Y, et al. Tofacitinib can decrease anti-DNA antibody titers in inactive systemic lupus erythematosus complicated by rheumatoid arthritis. Mod Rheumatol. 2016;26(4):633-4. doi: 10.3109/14397595.2015.1069473Yamamoto M, Yokoyama Y, Shimizu Y, et al. Tofacitinib can decrease anti-DNA antibody titers in inactive systemic lupus erythematosus complicated by rheumatoid arthritis. Mod Rheumatol. 2016;26(4):633-4. doi: 10.3109/14397595.2015.1069473Yamamoto M, Yokoyama Y, Shimizu Y, et al. Tofacitinib can decrease anti-DNA antibody titers in inactive systemic lupus erythematosus complicated by rheumatoid arthritis. Mod Rheumatol. 2016;26(4):633-4. doi: 10.3109/14397595.2015.1069473You H, Zhang G, Wang Q, et al. Successful treatment of arthritis and rash with tofacitinib in systemic lupus erythematosus: the experience from a single centre. Ann Rheum Dis. 2019 Apr 20. doi: 10.1136/annrheumdis-2019-215455You H, Zhang G, Wang Q, et al. Successful treatment of arthritis and rash with tofacitinib in systemic lupus erythematosus: the experience from a single centre. Ann Rheum Dis. 2019 Apr 20. doi: 10.1136/annrheumdis-2019-215455You H, Zhang G, Wang Q, et al. Successful treatment of arthritis and rash with tofacitinib in systemic lupus erythematosus: the experience from a single centre. Ann Rheum Dis. 2019 Apr 20. doi: 10.1136/annrheumdis-2019-215455You H, Zhang G, Wang Q, et al. Successful treatment of arthritis and rash with tofacitinib in systemic lupus erythematosus: the experience from a single centre. Ann Rheum Dis. 2019 Apr 20. doi: 10.1136/annrheumdis-2019-215455You H, Zhang G, Wang Q, et al. Successful treatment of arthritis and rash with tofacitinib in systemic lupus erythematosus: the experience from a single centre. Ann Rheum Dis. 2019 Apr 20. doi: 10.1136/annrheumdis-2019-215455You H, Zhang G, Wang Q, et al. Successful treatment of arthritis and rash with tofacitinib in systemic lupus erythematosus: the experience from a single centre. Ann Rheum Dis. 2019 Apr 20. doi: 10.1136/annrheumdis-2019-215455You H, Zhang G, Wang Q, et al. Successful treatment of arthritis and rash with tofacitinib in systemic lupus erythematosus: the experience from a single centre. Ann Rheum Dis. 2019 Apr 20. doi: 10.1136/annrheumdis-2019-215455You H, Zhang G, Wang Q, et al. Successful treatment of arthritis and rash with tofacitinib in systemic lupus erythematosus: the experience from a single centre. Ann Rheum Dis. 2019 Apr 20. doi: 10.1136/annrheumdis-2019-215455Wallace DJ, Furie RA, Tanaka Y, et al. Baricitinib for systemic lupus erythematosus: a double-blind, randomised, placebo-controlled, phase 2 trial. Lancet. 2018;392(10143):222-31. doi: 10.1016/S0140-6736(18)31363-1Wallace DJ, Furie RA, Tanaka Y, et al. Baricitinib for systemic lupus erythematosus: a double-blind, randomised, placebo-controlled, phase 2 trial. Lancet. 2018;392(10143):222-31. doi: 10.1016/S0140-6736(18)31363-1Wallace DJ, Furie RA, Tanaka Y, et al. Baricitinib for systemic lupus erythematosus: a double-blind, randomised, placebo-controlled, phase 2 trial. Lancet. 2018;392(10143):222-31. doi: 10.1016/S0140-6736(18)31363-1Wallace DJ, Furie RA, Tanaka Y, et al. Baricitinib for systemic lupus erythematosus: a double-blind, randomised, placebo-controlled, phase 2 trial. Lancet. 2018;392(10143):222-31. doi: 10.1016/S0140-6736(18)31363-1Wallace DJ, Furie RA, Tanaka Y, et al. Baricitinib for systemic lupus erythematosus: a double-blind, randomised, placebo-controlled, phase 2 trial. Lancet. 2018;392(10143):222-31. doi: 10.1016/S0140-6736(18)31363-1Wallace DJ, Furie RA, Tanaka Y, et al. Baricitinib for systemic lupus erythematosus: a double-blind, randomised, placebo-controlled, phase 2 trial. Lancet. 2018;392(10143):222-31. doi: 10.1016/S0140-6736(18)31363-1Wallace DJ, Furie RA, Tanaka Y, et al. Baricitinib for systemic lupus erythematosus: a double-blind, randomised, placebo-controlled, phase 2 trial. Lancet. 2018;392(10143):222-31. doi: 10.1016/S0140-6736(18)31363-1Wallace DJ, Furie RA, Tanaka Y, et al. Baricitinib for systemic lupus erythematosus: a double-blind, randomised, placebo-controlled, phase 2 trial. Lancet. 2018;392(10143):222-31. doi: 10.1016/S0140-6736(18)31363-1Zhang LJ. Type 1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis. Front Immunol. 2019;10:1440. doi: 10.3389/fimmu.2019.01440Zhang LJ. Type 1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis. Front Immunol. 2019;10:1440. doi: 10.3389/fimmu.2019.01440Zhang LJ. Type 1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis. Front Immunol. 2019;10:1440. doi: 10.3389/fimmu.2019.01440Zhang LJ. Type 1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis. Front Immunol. 2019;10:1440. doi: 10.3389/fimmu.2019.01440Zhang LJ. Type 1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis. Front Immunol. 2019;10:1440. doi: 10.3389/fimmu.2019.01440Zhang LJ. Type 1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis. Front Immunol. 2019;10:1440. doi: 10.3389/fimmu.2019.01440Zhang LJ. Type 1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis. Front Immunol. 2019;10:1440. doi: 10.3389/fimmu.2019.01440Zhang LJ. Type 1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis. Front Immunol. 2019;10:1440. doi: 10.3389/fimmu.2019.01440Mylonas A, Conrad C. Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon. Front Immunol. 2018;9:2746. doi: 10.3389/fimmu.2018.02746Mylonas A, Conrad C. Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon. Front Immunol. 2018;9:2746. doi: 10.3389/fimmu.2018.02746Mylonas A, Conrad C. Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon. Front Immunol. 2018;9:2746. doi: 10.3389/fimmu.2018.02746Mylonas A, Conrad C. Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon. Front Immunol. 2018;9:2746. doi: 10.3389/fimmu.2018.02746Mylonas A, Conrad C. Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon. Front Immunol. 2018;9:2746. doi: 10.3389/fimmu.2018.02746Mylonas A, Conrad C. Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon. Front Immunol. 2018;9:2746. doi: 10.3389/fimmu.2018.02746Mylonas A, Conrad C. Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon. Front Immunol. 2018;9:2746. doi: 10.3389/fimmu.2018.02746Mylonas A, Conrad C. Psoriasis: Classical vs. Paradoxical. The Yin-Yang of TNF and Type I Interferon. Front Immunol. 2018;9:2746. doi: 10.3389/fimmu.2018.02746Robinson ES, Werth VP. The role of cytokines in the pathogenesis of cutaneous lupus erythematosus. Cytokine. 2015;73:326-34. doi: 10.1016/j.cyto.2015.01.031Robinson ES, Werth VP. The role of cytokines in the pathogenesis of cutaneous lupus erythematosus. Cytokine. 2015;73:326-34. doi: 10.1016/j.cyto.2015.01.031Robinson ES, Werth VP. The role of cytokines in the pathogenesis of cutaneous lupus erythematosus. Cytokine. 2015;73:326-34. doi: 10.1016/j.cyto.2015.01.031Robinson ES, Werth VP. The role of cytokines in the pathogenesis of cutaneous lupus erythematosus. Cytokine. 2015;73:326-34. doi: 10.1016/j.cyto.2015.01.031Robinson ES, Werth VP. The role of cytokines in the pathogenesis of cutaneous lupus erythematosus. Cytokine. 2015;73:326-34. doi: 10.1016/j.cyto.2015.01.031Robinson ES, Werth VP. The role of cytokines in the pathogenesis of cutaneous lupus erythematosus. Cytokine. 2015;73:326-34. doi: 10.1016/j.cyto.2015.01.031Robinson ES, Werth VP. The role of cytokines in the pathogenesis of cutaneous lupus erythematosus. Cytokine. 2015;73:326-34. doi: 10.1016/j.cyto.2015.01.031Robinson ES, Werth VP. The role of cytokines in the pathogenesis of cutaneous lupus erythematosus. Cytokine. 2015;73:326-34. doi: 10.1016/j.cyto.2015.01.031Rubin RL. Drug-induced lupus. Expert Opin Drug Safe. 2015;14:361-78. doi: 10.1517/14740338.2015.995089Rubin RL. Drug-induced lupus. Expert Opin Drug Safe. 2015;14:361-78. doi: 10.1517/14740338.2015.995089Rubin RL. Drug-induced lupus. Expert Opin Drug Safe. 2015;14:361-78. doi: 10.1517/14740338.2015.995089Rubin RL. Drug-induced lupus. Expert Opin Drug Safe. 2015;14:361-78. doi: 10.1517/14740338.2015.995089Rubin RL. Drug-induced lupus. Expert Opin Drug Safe. 2015;14:361-78. doi: 10.1517/14740338.2015.995089Rubin RL. Drug-induced lupus. Expert Opin Drug Safe. 2015;14:361-78. doi: 10.1517/14740338.2015.995089Rubin RL. Drug-induced lupus. Expert Opin Drug Safe. 2015;14:361-78. doi: 10.1517/14740338.2015.995089Rubin RL. Drug-induced lupus. Expert Opin Drug Safe. 2015;14:361-78. doi: 10.1517/14740338.2015.995089Ciechanowicz P, Rakowska A, Sikora M, Rudnicka L. JAKinhibitors in dermatology. Current evidence and future applications. J Dermatolog Treat. 2018 Nov;15:1-22. doi: 10.1080/09546634.2018.1546043Ciechanowicz P, Rakowska A, Sikora M, Rudnicka L. JAKinhibitors in dermatology. Current evidence and future applications. J Dermatolog Treat. 2018 Nov;15:1-22. doi: 10.1080/09546634.2018.1546043Ciechanowicz P, Rakowska A, Sikora M, Rudnicka L. JAKinhibitors in dermatology. Current evidence and future applications. J Dermatolog Treat. 2018 Nov;15:1-22. doi: 10.1080/09546634.2018.1546043Ciechanowicz P, Rakowska A, Sikora M, Rudnicka L. JAKinhibitors in dermatology. Current evidence and future applications. J Dermatolog Treat. 2018 Nov;15:1-22. doi: 10.1080/09546634.2018.1546043Ciechanowicz P, Rakowska A, Sikora M, Rudnicka L. JAKinhibitors in dermatology. Current evidence and future applications. J Dermatolog Treat. 2018 Nov;15:1-22. doi: 10.1080/09546634.2018.1546043Ciechanowicz P, Rakowska A, Sikora M, Rudnicka L. JAKinhibitors in dermatology. Current evidence and future applications. J Dermatolog Treat. 2018 Nov;15:1-22. doi: 10.1080/09546634.2018.1546043Ciechanowicz P, Rakowska A, Sikora M, Rudnicka L. JAKinhibitors in dermatology. Current evidence and future applications. J Dermatolog Treat. 2018 Nov;15:1-22. doi: 10.1080/09546634.2018.1546043Ciechanowicz P, Rakowska A, Sikora M, Rudnicka L. JAKinhibitors in dermatology. Current evidence and future applications. J Dermatolog Treat. 2018 Nov;15:1-22. doi: 10.1080/09546634.2018.1546043

The authors declare that there are no conflicts of interest present.