Абатацепт при ревматоидном артрите: новая форма, новые механизмы, новые возможности
https://doi.org/10.14412/1995-4484-2015-522-541
Аннотация
Ревматоидный артрит (РА) – системное аутоиммунное ревматическое заболевание, характеризующееся хроническим воспалением синовиальной оболочки суставов и широким спектром внесуставных (системных) проявлений, ключевую роль в патогенезе которого играет патологическая активация Т-клеток. Поэтому среди разнообразных подходов к патогенетической терапии РА особое место занимает разработка препарата абатацепт (АБЦ), избирательно блокирующего костимуляцию Т-клеток. В обзоре представлены новые данные, касающиеся эффективности и безопасности подкожной лекарственной формы, обсуждены механизмы его действия в отношении подавления синтеза аутоантител, восстановления нормальной функции Т-регуляторных клеток и т. д. Специально рассмотрены механизмы, обеспечивающие синергическое действие АБЦ и метотрексата при РА, перспективы персонифицированной медицины в ревматологии на примере АБЦ.
Об авторе
Е. Л. Насонов
ФГБНУ Научно-исследовательский институт ревматологии им. В.А. Насоновой, Москва, Россия 115522 Москва, Каширское шоссе, 34А
Россия
Россия
директор ФГБНУ НИИР им. В.А. Насоновой, академик РАН, докт. мед. наук, профессор
Список литературы
1. Насонов ЕЛ, Каратеев ДЕ, Балабанова РМ. Ревматоидный артрит. В кн.: Насонов ЕЛ, Насонова ВА, редакторы. Ревматология. Национальное руководство. Москва: ГЭОТАР-Медиа; 2008. С. 290–331 [Nasonov EL, Karateev DE, Balabanova RM. Rheumatoid arthritis. In: Nasonov EL, Nasonova VA, editors. Revmatologiya. Natsional'noe rukovodstvo [Rheumatology. National guidelines]. Moscow: GEOTARMedia; 2008. P. 290–331].
2. McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. New Engl J Med. 2011;365:2205-19. doi: 10.1056/NEJMra1004965
3. Cho JH, Feldman M. Heterogeneity of autoimmune diseases: pathophysiologic insight from genetics and implications for new therapy. Nat Med. 2015;21:730–8. doi: 10.1038/nm.3897
4. Schett G, Elewaut D, McInnes JB, et al. How cytokine network fuel inflammation: toward a cytokine-based disease taxonomy. Nat Med. 2013;19:822–4. doi:10.1038/nm.3260
5. Насонов ЕЛ, редактор. Генно-инженерные биологические препараты в лечении ревматоидного артрита. Москва: ИМА-ПРЕСС; 2013. С. 549 [Nasonov EL, editor. Gennoinzhenernye biologicheskie preparaty v lechenii revmatoidnogo artrita [Genetically engineered biological agents in the treatment of rheumatoid arthritis]. Moscow: IMA-PRESS; 2013. P. 549].
6. Ceeraz S, Nowak EC, Burns CM, Noelle RJ. Immune checkpoint receptors regulating immune reactivity in rheumatic disease. Arthritis Res Ther. 2014;16:496. doi: 10.1186/s13075-014-0469-1
7. Padrol DM. The blockade on immune checkpoints in cancer immunotherapy. Nat Rev Immunol. 2012;12:252–64. doi: 10.1038/nrc3239
8. Chen L, Flies DB. Molecular mechanisms of T cell cо-stimulation and co-inhibition. Nat Rev Immunol. 2013;13:227–42. doi: 10.1038/nri3405
9. Romo-Tena J, Gomes-Martin D, Alcocer-Varela J. CTLA-4 and autoimmunity: new insight into the dual regulator of tolerance. Autoimmun Rev. 2013;12:1171–6. doi: 10.1016/j.autrev.2013.07.002
10. Sakaguchi S, Powrie F, Ransohoff RM. Re-establishing immunological self-tolerance in autoimmune disease. Nat Med. 2012;18:54. doi: 10.1038/nm.2622
11. Plenge RM, Padyukov L, Remmers EF, et al. Replication of putative candidate-gene associations with rheumatoid arthritis in >4,000 samples from North America and Sweden: association of susceptibility with PTPN22, CTLA4, and PADI4. Am J Hum Genet. 2005;77:1044–60. doi: 10.1086/498651
12. Flores-Borja F, Jury EC, Mauri C, Ehrenstein MR. Defects in CTLA-4 are associated with abnormal regulatory T cell function in rheumatoid arthritis. Proc Natl Acad Sci USA. 2008;105:19396–401. doi: 10.1073/pnas.0806855105
13. Cao J, Zou L, Luo P, et al. Increased production of circulating soluble co-stimulatory molecules CTLA-4, CD28 and CD80 in patients with rheumatoid arthritis. Int Immunopharmacol. 2012;14:585–92. doi: 10.1016/j.intimp.2012.08.004
14. Van de Ven K, Borst J. Targeting the T-cell co-stimulatory CD27/CD70 pathway in cancer immunotherapy: rationale and potential. Immunotherapy. 2015;7:655–67. doi: 10.2217/imt.15.32
15. Насонов ЕЛ, Каратеев ДЕ. Применение блокатора костимуляции Т-лимфоцитов абатацепта при ревматоидном артрите. Научно-практическая ревматология. 2010;4(приложение):9–27 [Nasonov EL, Karateev DE. Blockers costimulation of T-lymphocytes in rheumatoid arthritis abatacept. Nauchno-prakticheskaya revmatologiya =Rheumatology Science and Practice. 2010;4(Suppl):9–27 (In Russ.)].
16. Vicente Rabaneda EF, Herrero-Beaumont G, Castaneda S. Update on the use of abatacept for the treatment of rheumatoid arthritis. Expert Rev Clin Immunol. 2013;9:599–621. doi: 10.1586/1744666X.2013.811192
17. Schiff M, Bessette L. Evaluation of abatacept in biologic-naive patients with active rheumatoid arthritis. Clin Rheumatol. 2010;29:583–91. doi: 10.1007/s10067-009-1363-0
18. Keating GM. Abatacept: a review of its use in the management of rheumatoid arthritis. Drugs. 2013;73:1095–119. doi: 10.1007/s40265-013-0080-9
19. Schiff M. Subcutaneous abatacept for the treatment of rheumatoid arthritis. Rheumatology. 2013;52:986–97. doi: 10.1093/rheumatology/ket018
20. Wells AF, Jodat N, Schiff M. A critical evaluation of the role of subcutaneous abatacept in the treatment of rheumatoid arthritis: patients considerations. Biol Targ Ther. 2014;8:41–55. doi: 10.2147/BTT.S55783
21. Rakinen C, Conaghan PG. Comparative clinical utility of onceweekly subcutaneous abatacept in the management of rheumatoid arthritis. Therapeutics Clin Risk Manag. 2014;10:313–20.
22. Corbo M, Valencia X, Raymond R, et al. Subcutaneous administration of abatacept in patients with rheumatoid arthritis: Pharmacokinetics, safety and immunogenicity. Ann Rheum Dis. 2009;68(Suppl 3):574.
23. Genovese M, Covarrubias A, Leon G, et al. Subcutaneous abatacept versus intravenous abatacept: a phase IIIb noninferiority study in patients with an inadequate response to methotrexate. Arthritis Rheum. 2011;63:2854–64. doi: 10.1002/art.30463
24. Genovese MC, Tena CP, Covarrubias A, et al. Subcutaneous abatacept for the treatment of rheumatoid arthritis: long-term data from the ACQUIRE trial. J Rheumatol. 2014 Apr;41(4):629–39. doi: 10.3899/jrheum.130112
25. Kaine J, Gladstein G, Strusberg I, et al. Evaluation of abatacept administered subcutaneously in adults with active rheumatoid arthritis: impact of withdrawal and reintroduction on immunogenicity, efficacy and safety (phase IIIb ALLOW study). Ann Rheum Dis. 2012;71:38–44. doi: 10.1136/annrheumdis-2011- 200344
26. Keystone EC, Kremer JM, Russell A, et al. Abatacept in subjects who switch from intravenous to subcutaneous therapy: results from the phase IIIb ATTUNE study. Ann Rheum Dis. 2012;71:857–61. doi: 10.1136/annrheumdis-2011-200355
27. Nash P, Nayiager S, Genovese M, et al. Immunogenicity, safety and efficacy of subcutaneous abatacept with or without MTX in patients with rheumatoid arthritis: results from Phase III, international, multicenter, parallel-arm, open-label study. Arthritis Care Res (Hoboken). 2013;65:718–28. doi: 10.1002/acr.21876
28. Weinblatt M, Schiff M, Valente R, et al. Head-to-head comparison of subcutaneous abatacept versus adalimumab for rheumatoid arthritis: findings of a phase IIIb, multinational, prospective, randomized study. Arthritis Rheum. 2012;65:28–38. doi: 10.1002/art.37711
29. Schiff M, Weinblatt ME, Valente R, et al. Head-to-head comparison of subcutaneous abatacept versus adalimumab for rheumatoid arthritis: two-year efficacy and safety findings from AMPLE trial. Ann Rheum Dis. 2014;73:86–94. doi: 10.1136/annrheumdis-2013-203843
30. Emery P, Burmester GR, Bykerk V, et al. Evaluating drug-free remission with abatacept in early rheumatoid arthritis: results from the phase 3b multicenter, randomized, active-controlled AVERT study of 24 months, with a 12 months, double-blind treatment period. Ann Rheum Dis. 2015;74:19–26. doi: 10.1136/annrheumdis-2014-206106
31. Burmester G, Furst DE, Combe BG, et al. Stringent criteria for low disease activity and remission after 12 month of treatment, and after treatment withdrawal, with abatacept monotherapy, abatacept with methotrexate or methotrexate alone in early rheumatoid arthritis. Arthritis Rheum. 2014;66(Suppl):2468(abst).
32. Bykerk VP, Burmester GR, Combe BG, et al. On drug and drug-free remission by baseline disease duration in the avert trial: abatacept versus methotrexate comparison in patients with early rheumatoid arthritis. Ann Rheum Dis. 2015;74(Suppl 2):477–8. doi: 10.1136/annrheumdis-2015-eular.2071
33. Furs DE, Bykerk VP, Burmester G, et al. Patient-reported outcomes following 12 months of therapy with abatacept (plus methotrexate or as monotherapy) or methotrexate and up to 6 months after treatment withdrawal in patients with early rheumatoid arthritis. Arthritis Rheum. 2014;66(Suppl):2486(abst).
34. Emery P, Burmester G, Bykerk VH, et al. Predictors of drugfree remission following treatment with abatacept (in combination with methotrexate or as monotherapy) in early rheumatoid arthritis. Arthritis Rheum. 2014;66(Suppl):2485(abst).
35. Alten R, Kaine J, Keystone E, et al. Long-term safety of subcutaneous abatacept in rheumatoid arthritis. Integrated analysis of clinical trial data representing more than four years of treatment. Arthritis Rheum. 2014;66:1987–97. doi: 10.1002/art.38687
36. Jani M, Barton A, Warren R, et al. The role of DMARDs in reducing the immunogenicity of TNF inhibitors in chronic inflammatory diseases. Rheumatology. 2014;53:213–22. doi: 10.1093/rheumatology/ket260
37. Александрова ЕН, Насонов ЕЛ. Иммуногенность ингибиторов фактора некроза опухоли α при лечении ревматоидного артрита. Научно-практическая ревматология. 2012;50(приложение 4):22–7 [Aleksandrova EN, Nasonov EL. Immunogenicity inhibitors of tumor necrosis factor α in the treatment of rheumatoid arthritis. Nauchno-prakticheskaya revmatologiya =Rheumatology Science and Practice. 2012;50(Suppl 4):22–7 (In Russ.)].
38. Hochberg M, Janssen K, Broglio K, et al. Comparison of abatacept and other biologic DMARDs for the treatment of rheumatoid arthritis: a systemic literature review and network metaanalysis. Ann Rheum Dis. 2015;72(Suppl 4):678.
39. Fasth AE, Snir O, Johansson AA, et al. Skewed distribution of proinflammatory CD4+CD28null T cells in rheumatoid arthritis. Arthritis Res Ther. 2007;9:R87. doi: 10.1186/ar2286
40. Scarsi M, Zanotti C, Chiarini M, et al. Reduction of peripheral blood γ-IFN and IL-17 producing T cells after therapy with abatacept for rheumatoid arthritis. Clin Exp Rheumatol. 2014;32:204–10.
41. Schmidt D, Goronzy JJ, Weyand CM. CD4+CD7-CD28- T cells are expanded in rheumatoid arthritis and are characterized by autoreactivity. J Clin Invest. 1996;97:2027–37. doi: 10.1172/JCI118638
42. Vallejo AN, Weyand CM, Goronzy JJ. T-cell senescence: a culprit of immune abnormalities in chronic inflammation and persistent infection. Trends Mol Med. 2004;10:119–24. doi: 10.1016/j.molmed.2004.01.002
43. Broux B, Markovic-Plese S, Stinissen P, Hellings N. Pathogenic features of CD4+CD28- T cells in immune disorders. Trends Mol Med. 2012;18:446–53. doi: 10.1016/j.molmed.2012.06.003
44. Pawlik A, Ostanek L, Brzosko I, et al. The expansion of CD4+CD28- T cells in patients with rheumatoid arthritis. Arthritis Res Ther. 2003;5:R210–3. doi: 10.1186/ar766
45. Scarsi M, Ziglioli T, Airo' P. Baseline numbers of circulating CD28-negative T cells may predict clinical response to abatacept in patients with rheumatoid arthritis. J Rheumatol. 2011;38:2105–11. doi: 10.3899/jrheum.110386
46. Airo P, Scarsi M. Targeting CD4+CD28- T cells by blocking CD28 co-stimulation. Trends Mol Med. 2013;19:1–2. doi: 10.1016/j.molmed.2012.10.013
47. Koetz K, Bryl E, Spickschen K, et al. T cell homeostasis in patients with rheumatoid arthritis. Proc Natl Acad Sci USA. 2000;97:9203–8. doi: 10.1073/pnas.97.16.9203
48. Pierer M, Rossol M, Kaltenhä user S, et al. Clonal expansions in selected TCR BV families of rheumatoid arthritis patients are reduced by treatment with the TNFα inhibitors etanercept and infliximab. Rheumatol Int. 2011;31:1023–9. doi: 10.1007/s00296-010-1402-9
49. Fasth AE, Snir O, Johansson AA, et al. Skewed distribution of proinflammatory CD4+CD28null T cells in rheumatoid arthritis. Arthritis Res Ther. 2007;9:R87. doi: 10.1186/ar2286
50. Насонов ЕЛ, Александрова ЕН, Авдеева АС, Рубцов ЮП. Т-регуляторные клетки при ревматических заболеваниях. Научно-практическая ревматология. 2014;52:430–7 [Nasonov EL, Aleksandrova EN, Avdeeva AS, Rubtsov YuP. T-regulatory cells in rheumatic diseases. Nauchno-prakticheskaya revmatologiya =Rheumatology Science and Practice. 2014;52:430–7 (In Russ.)].
51. Alunno A, Manetti M, Caterbi S, et al. Altered immunoregulation in rheumatoid arthritis: the role of regulatory T cells and ptoinflammatory Th17 cells and their therapeutic implications. Mediators Inflamm. 2015;2015:751793. doi: 10.1155/2015/751793
52. Wehrens EJ, Prakken BJ, van Wijk F. T cells out of control – impaired immune regulation in the inflamed joint. Nat Rev Rheumatol. 2013;9:34–42. doi: 10.1038/nrrheum. 2012.149
53. Wing K, Onishi Y, Prieto-Martin P, et al. CTLA-4 control over Foxp3(+) regulatory T cell function. Science. 2008;322:271. doi: 10.1126/science.1160062
54. Walker LS. Treg and CTLA-4: Two intertwining pathways to immune tolerance. J Autoimmun. 2013;45:49. doi: 10.1016/j.jaut.2013.06.006
55. Onishi Y, Fehervari Z, Yamaguchi T, Sakaguchi S. Foxp3(+) natural regulatory T cells preferentially form aggregates on dendritic cells in vitro and actively inhibit their maturation. Proc Natl Acad Sci USA. 2008;3105:10113. doi: 10.1073/pnas.0711106105
56. Grohmann U, Orabona C, Fallarino F, et al. CTLA-4-Ig regulates tryptophan catabolism in vivo. Nat Immunol. 2002;3:1097. doi: 10.1038/ni846
57. Zheng Y, Manzotti CN, Liu M F, et al. CD86 and CD80 differentially modulate the suppressive function of human regulatory T cells. J Immunol. 2014;72:2778–84.
58. Cribbs P, Kennedy A, Penn H, et al. Treg cell function in rheumatoid arthritis is compromised by ctla-4 promoter methylation resulting in a failure to activate the indoleamine 2,3-dioxygenase pathway. Arthritis Rheum. 2014;66:2344–54. doi: 10.1002/art.38715
59. Bernard NJ. Rheumatoid arthritis: who knows why regulatory T cells are defective in RA. Nat Rev Rheumatol. 2014;10:381. doi: 10.1038/nrrheum.2014.96
60. Fallarino F, Grohmann U, Hwang KW, et al. Modulation of tryptophan catabolism by regulatory T cells. Nat Immunol. 2003;4:1206–12. doi: 10.1038/ni1003
61. Grohmann U, Orabona C, Fallarino F, et al. CTLA-4-Ig regulates tryptophan catabolism in vivo. Nat Immunol. 2001;3:1097–101. doi: 10.1038/ni846
62. Alvarez-Quiroga C, Abud-Mendoza C, Doniz-Padilla L, et al. CTLA-4-Ig therapy diminishes the frequency but enhances the function of Treg cells in patients with rheumatoid arthritis.J Clin Immunol. 2011;31:588–95. doi: 10.1007/s10875-011- 9527-5
63. Pieper J, Herrath J, Raghavan, SK, et al. CTLA4-Ig (abatacept) therapy modulates T cell effector functions in autoantibodypositive rheumatoid arthritis patients. BMC Immunol. 2013;14:34. doi: 10.1186/1471-2172-14-34
64. Picchianti Diamanti A, Rosado MM, Scarsella M, et al. Abatacept (cytotoxic T lymphocyte antigen 4-immunoglobulin) improves B cell function and regulatory T cell inhibitory apacity in rheumatoid arthritis patients non-responding to antitumour necrosis factor-α agents. Clin Exp Immunol. 2014;177:630–40. doi: 10.1111/cei.12367
65. Bedoya SK, Lam B, Lau K, Larkin J 3d. Th17 cells in immunity and autoimmunity. Clin Dev Immunol. 2013;2013:986789. doi: 10.1155/2013/986789
66. Насонов ЕЛ, Денисов ЛН, Станислав МЛ. Интерлейкин 17 – новая мишень для антицитокиновой терапии иммуновоспалительных ревматических заболеваний. Научно-практическая ревматология. 2013;51(5):545–52 [Nasonov EL, Denisov LN, Stanislav ML. Interleukin-17 is a new target for anti-cytokine therapy of immune inflammatory rheumatic diseases. Nauchno-prakticheskaya revmatologiya =Rheumatology Science and Practice. 2013;51(5):545–52 (In Russ.)]. doi: 10.14412/1995-4484-2013-1547
67. Singh RP, Hasan S, Sharma S, et al. Th17 cells in inflammation and autoimmunity. Autoimmun Rev. 2014;13:1174–81. doi: 10.1016/j.autrev.2014.08.019
68. Matsutani T, Li Y, Murakami M, et al. Abatacept (CTLA4-Ig) suppresses T cell activation and reduces TH17 cells as well as plasma IL-6 in patients with rheumatoid arthritis. Ann Rheum Dis. 2013;73:383. doi: 10.1136/annrheumdis-2012-eular.2663
69. Murakami M, Matsutani T, Sekiguchi M, et al. Changes in cytokine profiles in rheumatoid arthritis patients during abatacept treatment. Ann Rheum Dis. 2013;72:A622. doi: 10.1136/annrheumdis-2013-eular.1847
70. Golding SR. Inflammatory signaling induced bone lose. Bone. 2015 May 28. doi: 10.1016/j.bone.2015.05.024
71. Schett G, Gravallese E. Bone erosion in rheumatoid arthritis: mechanism, diagnosis and treatment. Nat Rev Rheumatol. 2012;8:656–64. doi: 10.1038/nrrgeum.2012.153
72. Grassi F, Tell G, Robbie-Ryan M, et al. Oxidative stress causes bone loss in estrogen-deficient mice through enhanced bone marrow dendritic cell activation. Proc Natl Acad Sci USA. 2007;104:15087–92. doi: 10.1073/pnas.0703610104
73. Bedi B, Li JY, Grassi F, et al. Inhibition of antigen presentation and T cell costimulation blocks PTH-induced bone loss. Ann NY Acad Sci. 2010;1192:215–21. doi: 10.1111/j.1749- 6632.2009.05216.x
74. Axmann R, Herman S, Zaiss M, et al. CTLA-4 directly inhibits osteoclast formation. Ann Rheum Dis. 2008;67:1603–9. doi: 10.1136/ard.2007.080713
75. Roser-Page S, Vikulina T, Zayzafoon M, Weitzmann MN. CTLA-4Ig-induced T cell anergy promotes Wnt-10b production and bone formation in a mouse model. Arthritis Rheum. 2014;66:990–9. doi: 10.1002/art.38319
76. Leandro M. B cells and rheumatoid factors in autoimmunity. Int J Rheum Dis. 2015;18:379–81. doi: 10.1111/1756-185X.12690
77. Dö rner T, Jacobi AM, Lipsky PE. B cells in autoimmunity. Arthritis Res Ther. 2009;11:247. doi: 10.1186/ar2780
78. Mastrangelo A, Colasanti T, Barbati C, et al. The role of posttranslational protein modifications in rheumatological diseases: focus on rheumatoid arthritis. J Immunol Res. 2015. doi: 10.1155/2015/712490
79. Anzilotti C, Pratesi F, Tommasi C, Migliorini P. Peptidylarginine deiminase 4 and citrullination in health and disease. Autoimmun Rev. 2010;9:158–60. doi: 10.1016/j.autrev.2009.06.002
80. Darrah E, Andrade F. Citrullination, and carbamylation, and malondialdehyde-acetaldehyde! Oh My! Entering the forest of autoantigen modifications in rheumatoid arthritis. Arthritis Rheum. 2015;67:604–8. doi: 10.1002/art.38970
81. Trouw LA, Mahler M. Closing the serological gap: promising novel biomarkers for the early diagnosis of rheumatoid arthritis. Autoimmun Rev. 2012;12:318–22. doi: 10.1016/j.autrev.2012.05.007
82. Willemze A, Trouw LA, Toes RE, Huizinga TWJ. The influence of ACPA status and characteristics on the course of RA. Nat Rev Rheumatol. 2012;8:114–52. doi: 10.1038/nrrheum.2011;204
83. Klareskof L, Amara K, Malmstrom V. Adaptive immunity in rheumatoid arthritis: anticitrulline and other antibodies in the pathogenesis of rheumatoid arthritis. Curr Opin Rheumatol. 2014;26:72–9. doi: 10.1097/BOR.0000000000000016
84. Nishimura K, Sugiyama D, Kogata Y, et al. Meta-analysis: diagnostic accuracy of anti-cyclic citrullinated peptide antibody and rheumatoid factor for rheumatoid arthritis. Ann Intern Med. 2007;146:797–808. doi: 10.7326/0003-4819-146-11-200706050- 00008
85. Новиков АА, Александрова ЕН, Черкасова МВ, Насонов ЕЛ. Современные методы лабораторной диагностики ревматоидного артрита. Научно-практическая ревматология. 2010;(1):31–45 [Novikov AA, Aleksandrova EN, Cherkasova MV, Nasonov EL. Modern methods of laboratory diagnosis of rheumatoid arthritis. Nauchnoprakticheskaya revmatologiya =Rheumatology Science and Practice. 2010;(1):31–45 (In Russ.)].
86. Taylor P, Gartemann J, Hsieh J, Greeden J. A systemic review of serum biomarkers anti-cyclic citrullinated peptide and rheumatoid factor as test for rheumatoid arthritis. Autoimmune Dis. 2011;2011:815038. doi: 10.4061/2011/815038
87. Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010;62:2569–81. doi: 10.1002/art.27584
88. Nielen MM, van Schaardenburg D, Reesink HW, et al. Specific autoantibodies precede the symptoms of rheumatoid arthritis: a study of serial measurements in blood donors. Arthritis Rheum. 2004;50:380–6. doi: 10.1002/art.20018
89. Arkema EV, Goldstein BL, Robinson W, et al. Anti-citrullinated peptide autoantibodies, human leukocyte antigen shared epitope and risk of future rheumatoid arthritis: a nested case-control study. Arthritis Res Ther. 2013;15:R159. doi: 10.1186/ar4342
90. Jilani AA, Mackworth-Young CG. The role of citrullinated protein antibodies in predicting erosive disease in rheumatoid arthritis: a systemic literature review and meta-analysis. Int J Rheumatol. 2015;2015:Article ID 728610. doi: 10.1155/2015/728610
91. Kuller LH, Mackey RH, Walitt BT, et al. Determinants of mortality among postmenopausal women in the Women's health initiative who report rheumatoid arthritis. Arthritis Rheum. 2014;66:497–507. doi: 10.1002/art.38268
92. Humphreys J, van Nies JAB, Chupping J, et al. Rheumatoid factor and anti-citrullinated protein antibody positivity, but not level, are associated with increased mortality in patients with rheumatoid arthritis: results from two large independent cohort. Arthritis Res Ther. 2014;16:483. doi: 10.1186/s13075-014-0483-3
93. Sakkas LI, Bogdanos DP, Katsiari C, Platsoucas CD. Anti-citrullinated peptide as autoantigen in rheumatoid arthritis – relevance to treatment. Autoimmune Rev. 2014;13:1114–20. doi: 10.1016/j.autrev.2014.08.012
94. Klareskog L, Catrina AI, Paget S. Rheumatoid arthritis. Lancet. 2009;373:659–72. doi: 10.1016/S0140-6736(09)60008-8
95. Ioan-Facsinay A, el-Bannoudi H, Scherer HU, et al. Anti-cyclic citrullinated peptide antibodies are a collection of anti-citrullinated protein antibodies and contain overlapping and non-overlapping reactivities. Ann Rheum Dis. 2011;70:188–93. doi: 10.1136/ard.2010.131102
96. Uysal H, Bockermann R, Nandakumar KS, et al. Structure and pathogenicity of antibodies specific for citrullinated collagen type II in experimental arthritis. J Exp Med. 2009;206:449–62. doi: 10.1084/jem.20081862
97. Amara K, Steen J, Murray F, et al. Monoclonal IgG antibodies generated from joint-derived B cells of RA patients have a strong bias toward citrullinated autoantigen recognition. J Exp Med. 2013;210:445–55. doi: 10.1084/jem.20121486
98. Cornaby C, Gibbons L, Mayhew V, et al. B cell epitope spreading: mechanism and contribution to autoimmune diseases. Immunol Let. 2015;163:56–68. doi: 10.1016/j.imlet.2014.11.001
99. Van de Stadt LA, de Koning MH, van de Stadt RJ, et al. Development of the anti-citrullinated protein antibody repertoire prior to the onset of rheumatoid arthritis. Arthritis Rheum. 2011;63:3226–33. doi: 10.1002/art.30537
100. Van der Woude D, Rantapaa-Dahlqvist S, Ioan-Facsinay A, et al. Epitope spreading of the anti-citrullinated protein antibody response occurs before disease onset and is associated with the disease course of early arthritis. Ann Rheum Dis. 2010;69:1554–61. doi: 10.1136/ard.2009.124537
101. Willemze A, Shi J, Mulder M, et al. The concentration of anticitrullinated protein antibodies in serum and synovial fluid in relation to total immunoglobulin concentrations. Ann Rheum Dis. 2013;72:1059–63. doi: 10.1136/annrheumdis-2012-202747
102. Fisher BA, Plant D, Brode M, et al. Antibodies to citrullinated alpha-enolase peptide 1 and clinical and radiological outcomes in rheumatoid arthritis. Ann Rheum Dis. 2011;70:1095–8. doi: 10.1136/ard.2010.138909
103. Willemze A, Bohringer S, Knevel R, et al. The ACPA recognition profile and subgrouping of ACPA-positive RA patients. Ann Rheum Dis. 2012;71:268–74. doi: 10.1136/annrheumdis-2011-200421
104. Ioan-Facsinay A, Willemze A, Robinson DB, et al. Marked differences in fine specificity and isotype usage of the anti-citrullinated protein antibody in health and disease. Arthritis Rheum. 2008;58:3000–8. doi: 10.1002/art.23763
105. Kokkonen H, Mullazehi M, Berglin E, et al. Antibodies of IgG, IgA and IgM isotypes against cyclic citrullinated peptide precede the development of rheumatoid arthritis. Arthritis Res Ther. 2011;13:R13. doi: 10.1186/ar3237
106. Van der Woude D, Syversen SW, van der Voort EI, et al. The ACPA isotype profile reflects long-term radiographic progression in rheumatoid arthritis. Ann Rheum Dis. 2010;69:1110–6. doi: 10.1136/ard.2009.116384
107. Suwannalai P, Scherer HU, van der Woude D, et al. Anti-citrullinated protein antibodies have a low avidity compared with antibodies against recall antigens. Ann Rheum Dis. 2011;70:373–9. doi: 10.1136/ard.2010.135509
108. Suwannalai P, van de Stadt LA, Radner H, et al. Avidity maturation of anti-citrullinated protein antibodies in rheumatoid arthritis. Arthritis Rheum. 2012;64:1323–8. doi: 10.1002/art.33489
109. Goulabchand R, Vincent T, Batteux F, et al. Impact of autoantibody glycosylation in autoimmune disease. Autoimmune Rev. 2014;13:742–50. doi: 10.1016/j.autrev.2014.02.005
110. Scherer HU, Wang J, Toes RE, et al. Immunoglobulin 1 (IgG1) Fc-glycosylation profiling of anti-citrullinated peptide antibodies from human serum. Proteomics Clin Appl. 2009;3:106–15. doi: 10.1002/prca.200800098
111. Scherer HU, van der Woude D, Ioan-Facsinay A, et al. Glycan profiling of anti-citrullinated protein antibodies isolated from human serum and synovial fluid. Arthritis Rheum. 2010;62:1620–9. doi: 10.1002/art.27414
112. Rombouts Y, Ewing E, van de Stadt LA, et al. Anti-citrullinated protein antibodies acquire a pro-inflammatory Fc glycosylation phenotype prior to the onset of rheumatoid arthritis. Ann Rheum Dis. 2015;74:234–41. doi: 10.1136/annrheumdis-2013-203565
113. Arnold JN, Wormald MR, Sim RB, et al. The impact of glycosylation on the biological function and structure of human immunoglobulins. Ann Rev Immunol. 2007;25:21–50. doi: 10.1146/annurev.immunol.25.022106.141702
114. Stadlmann J, Pabst M, Altmann F. Analytical and functional aspects of antibody sialylation. J Clin Immunol. 2010;30:15–9. doi: 10.1007/s10875-010-9409-2
115. Clavel C, Nogueira L, Laurent L, et al. Induction of macrophage secretion of tumor necrosis factor alpha through Fc gamma receptor IIa engagement by rheumatoid arthritis-specific autoantibodies to citrullinated proteins complexed with fibrinogen. Arthritis Rheum. 2008;58:678–88. doi: 10.1002/art.23284
116. Sokolove J, Zhao X, Chandra PE, Robinson WH. Immune complexes containing citrullinated fibrinogen costimulate macrophages via Toll-like receptor 4 and Fc gamma receptor. Arthritis Rheum. 2011;63:53–62. doi: 10.1002/art.30081
117. Kuhn KA, Kulik L, Tomooka B, et al. Antibodies against citrullinated proteins enhance tissue injury in experimental autoimmune arthritis. J Clin Invest. 2006;116:961–73. doi: 10.1172/JCI25422
118. Uysal H, Bockermann R, Nandakumar KS, et al. Structure and pathogenicity of antibodies specific for citrullinated collagen type II in experimental arthritis. J Exp Med. 2009;206:449–62. doi: 10.1084/jem.20081862
119. Trouw LA, Haisma EM, Levarht W, et al. Anti-cyclic citrullinated peptide antibodies from rheumatoid arthritis patients activate complement via both the classical and alternative pathways. Arthritis Rheum. 2009;60:1923–31. doi: 10.1002/art.24622
120. Sokolove J, Johnson DS, Lahey LJ, et al. Rheumatoid factor as a potentiator of anti-citrullinated protein antibody-mediated inflammation in rheumatoid arthritis. Arthritis Rheum. 2014;66:813–21. doi: 10.1002/art.38307
121. Laurent L, Anqurti F, Clavel C, et al. IgM rheumatoid factor amplifies the inflammatory response of macrophages induced by the rheumatoid arthritis-specific immune complexes containing anticitrullinated protein antibodies. Ann Rheum Dis. 2014. doi: 10/1136/annrheumdis-2013-204543
122. Hecht C, Englbrecht M, Rech J, et al. Additive effect of anticitrullinated protein antibodies and rheumatoid factor on bone erosions in patients with RA. Ann Rheum Dis. 2014. doi: 10.1136/annrheumdis-2014-205428
123. Harre U, Georgess D, Bang H, et al. Induction of osteoclastogenesis and bone loss by human autoantibodies against citrullinated vimentin. J Clin Invest. 2012;122:1791–802. doi: 10.1172/JCI60975
124. Harre U, Lang SC, Pfeifle R, et al. Glycosylation of immunoglobulin G determines osteoclast differentiation and bone lose. Nat Commun. 2015;6:6651. doi: 10.1038/ncomms7651
125. Kleyer A, Finsel S, Rech J, et al. Bone loss before the clinical onset of rheumatoid arthritis in subjects with anticitrullinated protein antibodies. Ann Rheum Dis. 2014;73:854–60. doi: 10.1136/annrhgeumdis-2012-202958
126. Dwivedi N, Radic M. Citrullination of autoantigens implicated NETosis in the induction of autoimmunity. Ann Rheum Dis. 2014;73:483–91. doi: 10.1136/annrheumdis-2013-203844
127. Khandpur R, Camona-Rivera C, Vivekanandan-Giri A, et al. NETs are source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis. Sci Transl Med. 2013;5:178ra40. doi: 10.1126/scitranslmed.3005580
128. Mocsai A, Ruland J, Tybulewicz VL. The SYK tyrosine kinase: a crucial player in diverse biological functions. Nat Rev Immunol. 2010;10:387–402. doi: 10.1038/nri2765
129. Iwata S, Yamaoka K, Niiro H, et al. Amplification of Toll-like receptor-mediated signaling through spleen tyrosine kinase in human B-cell activation. J Allergy Clin Immunol. 2012;129:1594–601. doi: 10.1016/j.jaci.2012.03.014
130. Iwata S, Nakayamada S, Fukuyo S, et al. Activation of Syk in peripheral blood B cells in patients with rheumatoid arthritis. A potential target for abatacept therapy. Arthritis Rheum. 2015;67:63–73. doi: 10.1002/art.38895
131. Crotty S. Follicular helper CD4 T cells (TFH). Ann Rev Immunol. 2011;29:621–63. doi: 10.1146/annurev-immunol-031210-101400
132. Platt AM, Gibson VB, Patakas A, et al. Abatacept limits breach of self-tolerance in a murine model of arthritis via effects on the generation of T follicular helper cells. J Immunol. 2010;185:1558–67. doi: 10.4049/jimmunol.1001311
133. Jansen D, el Bannoudi H, Arens R, et al. Abatacept decreases disease activity in the absence of CD4+ T-cells in the collagen induced arthritis model. Arthritis Res Ther. 2015;17:220. doi: 10.1186/s13075-015-0731-1
134. Cutolo M, Nadler SG. Advances in CTLA-4-IgG-mediated modulation of inflammatory cell and immune response activation in rheumatoid arthritis. Autoimmun Rev. 2013;12:758–67. doi: 10.1016/j.autrev.2013.01.001
135. Isaacs JD, Cohen SB, Emery P, et al. Effect of baseline rheumatoid factor and anticitrullinated peptide antibody serotype on rituximab clinical response: a meta-analysis. Ann Rheum Dis. 2013;72(3):329–36. doi: 10.1136/annrheumdis-2011-201117
136. Maneiro RJ, Salfado E, Carmona L, Gomez-Reino JJ. Rheumatoid factor as predictor of response to abatacept, rituximab and tocilizumab in rheumatoid arthritis: systemic review and meta-analysis. Semin Arthritis Rheum. 2013;43:9–17. doi: 10.1016/j.semarthrit.2012.11.007
137. Lv Q, Yin Y, Li X, et al. The status of rheumatoid factor and anti-cyclic citrullinated peptide antibody are not associated with the effect of anti-TNFα agent treatment in patients with rheumatoid arthritis: a meta-analysis. PloS One. 2014;27(9):e89442. doi: 10.1371/journal.pone.0089442
138. Kremer JM, Dougados M, Emery P, et al. Treatment of rheumatoid arthritis with the selective costimulation modulator abatacept: twelve-month results of a phase IIb, double-blind, randomized, placebo-controlled trial. Arthritis Rheum. 2005;52:2263–71. doi: 10.1002/art.21201
139. Schiff M, Keiserman M, Codding C, et al. Efficacy and safety of abatacept or infliximab vs placebo in ATTEST: a phase III, multi-centre, randomised, double-blind, placebo-controlled study in patients with rheumatoid arthritis and an inadequate response to methotrexate. Ann Rheum Dis. 2008;67:1096–103. doi: 10.1136/ard.2007.080002
140. Sokolove J, Schiff M, Fleiscmann R, et al. Effect of baseline anti-cyclic citrullinated peptide 2 antibody titre on patientreported outcome following treatment with subcutaneous abatacept or adalimumab. Ann Rheum Dis. 2015;72(Suppl 4):675. doi: 10.1136/annrhreumdis-eular.2215
141. Sokolove J, Schiff M, Fleiscmann R, et al. Impact of baseline anti-cyclic citrullinated peptide 2 antibody titre on efficacy outcome following treatment with subcutaneous abatacept or adalimumab: 2-year results from the AMPLE trial. Ann Rheum Dis. 2015;72(Suppl 4):675. doi: 10.1136/annrhreumdiseular. 1790
142. Huizinga TWG, Connolly SE, Johnsen A, et al. Effect of anticyclic citrullinated peptide 2 immunoglobulin M serostatus on efficacy outcomes following treatment with abatacept plus methotrexate in the avert trial. Ann Rheum Dis. 2015;74(Suppl 2):234–5. doi: 10.1136/annrheumdis-2015-eular.1983
143. Fujii T, Sekiguchi M, Matsui K, et al. Very high titer of anti-citrullinated protein antibodies is associated with the achievement of clinical remission by abatacept in biologic-naive patients with rheumatoid arthritis. (the ABROAD study). Ann Rheum Dis. 2013;72:A889. doi: 10/1135/annrheumdis-2013-eular.2656
144. Sekiguchi M, Fujii T, Kitano M, et al. Predicting factors associated with sustained clinical remission by abatacept are different between younger and eldery patients with biologic-naive rheumatoid arthritis (ABROAD study). Ann Rheum Dis. 2015;72(Suppl 4):1056. doi: 10.1136/annrheumdis-2015-eular.2693
145. Takahashi N, Kojima T, Funahashi K, et al. Positivity for rheumatoid factor associated with a better short-term response and long-term drug retention of abatacept: results from consecutive 508 patients with rheumatoid arthritis in a Japanese multicenter registry. Ann Rheum Dis. 2015;72(Suppl 4):488. doi: 10.1136/annrhreumdis-eular.2120
146. Gottenberg JE, Neto D, Gomez-Reino J, et al. Positivity for rheumatoid factor and anti-cyclic citrullinated peptide is associated with better drug retention of abatacept: a data from a Paneuropean analysis of RA register. Ann Rheum Dis. 2014;72(Suppl 2):505. doi: 10.1136/annrheumdis-2014-eular.5345
147. Van Dongen H, van Aken J, Lard LR, et al. Efficacy of methotrexate treatment in patients with probable rheumatoid arthritis – double-blind, randomized, placeb0-controlled trial. Arthritis Rheum. 2007;56:1421–32. doi: 10.1002/art.22525
148. Visser K, Verpoort KN, van Dongen H, et al. Pretreatment serum levels 0f anti-cyclic citrullinated peptide antibodies are associated with the response to methotrexate in recent-onxet arthritis. Ann Rheum Dis. 2008;67:1194–5. doi: 10.1136/ard.2008.088070
149. Huizinga TWJ, Connolly SE, Furst DE, et al. The impact of anti-citrullinated protein antibody isotypes and fine specificity in patients with early RA treated with abatacept and methotrexare. Arthritis Rheum. 2014;66 (Suppl):1515(abst).
150. Connolly S, Maldonado M, Schiff M, et al. Modulation of the ACPA fine specificity in patients with RA treated with either abatacept or adalimumab in the AMPLE study. Ann Rheum Dis. 2015;72(Suppl 4):395. doi: 10.1136/annrhreumdis-eular.2469
151. Anno S, Inui K, Mamoto K, et al. Abatacept might not alter anti-cyclic citrullinated peptide levels in established rheumatoid arthritis – AIRTIGHT study. Ann Rheum Dis. 2015;72(Suppl 4):1058. doi: 10.1136/annrhreumdis-eular.3779
152. Ramos-Casals M, Roberto-Perez-Alvarez, Diaz-Lagares C, et al. Autoimmune diseases induced by biological agents: a doubleedged sword? Autoimmun Rev. 2010;9:188–93. doi: 10.1016/j.autrev.2009.10.003
153. Buch MH, Johnsen A, Wong DA, Schiff M. Can anti-TNFinduced autoantibody conversion be reversed by switching to abatacept therapy in patients with RA on background MTX? Ann Rheum Dis. 2015;72(Suppl.4):675. doi: 10.1136/annrhreumdis-eular.1497
154. Scarsi M, Paolini L, Ricotta D, et al. Abatacept reduces levels of switched memory B cells, autoantibodies, and immunoglobulins in patients with rheumatoid arthritis. J Rheumatol.2014;41:666–72. doi: 10.3899/jrheum.130905
155. Huiziga TWJ, Emery P, Westhovens R, et al. Rate of anti-cyclic citrullinated peptide antibody and rheumatoid factor seroconversion in patients with undifferentiated arthritis or early rheumatoid arthritis treated with abatacept. Arthritis Rheum. 2011;2232(abst).
156. Modi S, Soejima M, Levesque MC. The effect of targeted rheumatoid arthritis therapies on anti-citrullinated protein autoantibody levels and B cell responses. Clin Exp Immunol. 2013;173:8–17. doi: 10.1111/cei.12114
157. Bohler C, Radner H, Smolen JS, Aletaha D. Serological changes in the course of traditional and biological disease modifying therapy of rheumatoid arthritis. Ann Rheum Dis. 2013;72:241–4. doi: 10.1136/annrheumdis-2012-202297
158. Van Vollenhoven RF, Geborek P, Forslind K, et al. Conventional combination treatment versus biological treatment in methotrexate-refractory early rheumatoid arthritis: 2 year ollow- up of the randomised, non-blinded, parallel-group Swefot trial. Lancet. 2012;379:1712–20. doi: 10.1016/S0140-6736(12)60027-0
159. Kastbom A, Forslind K, Ernestam S, et al. Changes in the anticitrullinated peptide antibody response in relation to therapeutic outcome in early rheumatoid arthritis: results the SWEFOT trial. Ann Rheum Dis. 2014. doi: 10.1136/annrheumdis-2014-205698
160. Ally MMTM, Hodkinson B, Meyer PWA, et al. Circulating anti-citrullinated peptide antibodies, cytokines and genotype as biomarkers of response to disease-modifying antirheumatic druf therapy in early rheumatoid arthritis. BMC Musculoskeletal Dis. 2015;16:130. doi: 10.1186/s12891-015-0587-1
161. Barra L, Bykerk V, Pope JE, et al. Anticitrullinated protein antibodies and rheumatoid factor fluctuate in early inflammatory arthritis and not predict clinical outcome. J Rheumatol. 2013;40:1259–67. doi: 10.3899/jrheumtol.120736
162. Bandyopadhyay S, Maldonado M, Schiff M, et al. Gene expression analyses of abatacept- and adalimumab-treated patients from the ample trial. Arthritis Rheum. 2014;66(Supp):1520(abst).
163. Derambure C, Vittecoq O, Dzangue Tchoupou G, et al. Analysis of gene expression fluctuation with abatacept pathway as a mechanism of action of abatacept in rheumatoid arthritis. Arthritis Rheum. 2012;64(Suppl):1517(abst).
164. Verbrugge SE, Scheper RJ, Lems WF, et al. Proteasome inhibitors as experimental therapeutics of autoimmune diseases. Arthritis Res Ther. 2015;17:17. doi: 10.1186/s13075-015-0529-1
165. Obry A, Cosette P, Lequerre T, et al. Protein quantification using mass spectrometry methods to predict response to abatacept and methotrexate combination therapy in rheumatoid arthritis. Arthritis Rheum. 2012;64(Suppl);2923(abst).
166. Smolen JS, Landewe R, Breedveld FC, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2013 update. Ann Rheum Dis. 2014;73:492–509. doi: 10.1136/annrheumdis-2013-204573
167. Smolen JS, Breedvald FC, Burmester GR, et al. Treating rheumatoid arthritis to target: 2014 update of the recommendations of an international task force. Ann Rheum Dis. 2015; doi:10.1036/annrheumdis-2015-32075242014
168. Насонов ЕЛ, Мазуров ВИ, Каратеев ДЕ и др. Проект рекомендаций по лечению ревматоидного артрита Общероссийской общественной организации «Ассоциация ревматологов России» – 2014 (часть 1). Научно-практическая ревматология. 2014;52(5):477–94 [Nasonov EL, Mazurov VI, Karateev DE, et al. Spondyloarthritis: Evolution of a concept. Project: recommendations on treatment of rheumatoid arthritis developed by All-Russian Public organization «Association of Rheumatologists of Russia» – 2014 (part 1). Nauchno-prakticheskaya revmatologiya =Rheumatology Science and Practice. 2014;52(5):477–94 (In Russ.)]. doi: 10.14412/1995-4484-2014-477-494
169. Buckley F, Finckh A, Huizinga TWJ, et al. Comparative efficacy of novel DMARDs as monotherapy and in combination with methotrexate in rheumatoid arthritis patients with inadequate response to conventional DMARDs: a network meta-analysis. J Man Care Spec Pharm. 2015;21:409–23.
170. Jorgensen TS, Tarp S, Furst DE, et al. Added-value of combining methotrexate with a biological agent compared to biological monotherapy in patients with rheumatoid arthritis: a systemic review and meta-analysis of randomized trials. Ann Rheum Dis. 2015;74(Suppl2):239. doi: 10.1136/annrheumdis-2015-eular.3396
171. Striesow F, Brandt A. Preference, satisfaction and usability of subcutaneous administrered methotrexate for rheumatoid arthritis or psoriatic arthritis: results of a postmarketing surveillance study with a high-concentration formulation. Ther Adv Musculoskeletal Dis. 2012;4:3–9. doi: 10.1177/1759720X11431004
172. Насонов ЕЛ. Метотрексат при ревматоидном артрите –2015: новые факты и идеи. Научно-практическая ревматология. 2015;53(4):421–33 [Nasonov EL. Methotrexate in heumatoid arthritis – 2015: New facts and ideas. Nauchnoprakticheskaya revmatologiya = Rheumatology Science and Practice. 2015;53(4):421–33 (In Russ.)]. doi: 10.14412/1995- 4484-2015-421-433.
173. Malavia AP, Ostor AJK. Drug adherence to biologic DMARDs with a special emphasis on the benefits of subcutaneous abatacept. Patients Pref Adher. 2012;6:589–96.
174. Smolen JS, Aletaha D. Rheumatoid arthritis therapy reappraisal: strategies, opportunities and challenges. Nat Rev Rheumatol. 2015;11(5):276–89. doi: 10.1038/nrrheum.2015.8
175. Westhovens R, Robles M, Ximenes AC, et al. Maintenance of remission following 2 years of standart treatment then dose reduction with abatacept in patients with early rheumatoid arthritis and poor prognosis. Ann Rheum Dis. 2015;74:564–8. doi: 10.1136/annrheumdis-2014-206149
176. Westhovens R, Robles M, Ximenes AC, et al. Clinical efficacy and safety of abatacept in methotrexate-naive patients with early rheumatoid arthritis and poor prognostic factors. Ann Rheum Dis. 2009;68:1870–7. doi: 10.1136/ard.2008.101121
177. Felson DT, Smolen JS, Wells G, et al. American College of Rheumatology/European League Against Rheumatism Provisional definition of remission in rheumatoid arthritis for clinical trials. Ann Rheum Dis. 2011;70:404–13. doi: 10.1136/ard.2011.149765
178. Cribbs AP, Kennedy A, Penn H, et al. Methotrexate restores regulatory T cell function through demethelation of the FoxP3 upstream enhancer in patients with rheumatoid arthritis. Arthritis Rheum. 2015;67:1182–92. doi: 10.1002/art.39031
179. Chan ESL, Cronstein BN. Methotrexate – how does it really work? Nat Rev Rheumatol. 2010;6,175–8. doi: 10.1038/nrrheum.2010.5
180. Ohta A, Sitkovsky M. Extracellular adenosine-mediated modulation of regulatory T cells. Front Immunol. 2014;5:1–9. doi: 10.3389/fimmu.2014.00304
181. Glaesener S, Quach TD, Onken N, et al. Distinct effects of methotrexate and etanercept on the B cell compartment in patients with juvenile idiopathic arthritis. Arthritis Rheum. 2014;66:2590–600. doi: 10.1002/art.38736
182. Tussiwand R, Bosco N, Ceredig R, Rolink AG. Tolerance checkpoints in B-cell development: Johny B good. Eur J Immunol. 2009;39:2317–8. doi: 10.1002/eji.200939633
183. Bohm I. Decrease of B-cells and autoantibodies after low-dose methotrexate. Biomed Pharmacol. 2003;57:278–82. doi: 10.1016/S0753-3322(03)00086-6
184. Coffey G, Betz A, Graf J, et al. Methotrexate and spleen tyrosine kinase inhibitor cooperate to inhibit responses to peripheral blood B cells in rheumatoid arthritis. Pharm Res Per. 2013 Dec;1(2):e00016. doi: 10.1002/prp2.16
185. Rozanski CH, Arens R, Carlson LM, et al. Sustained antibody responses depends on CD28 function in bone marrow-resident plasma cells. J Exp Med. 2011;208:1435–46. doi: 10.1084/jem.20110040
186. Scarsi M, Zilioli T, Airo P. Baseline numbers of circulating CD28-negative T cells may predict clinical response to abatacept in patients with rheumatoid arthritis. J Rheumatol. 2011;38:2105–11. doi: 10.3899/jrheum.110386
187. Kuehn HS, Ouyang W, Lo B, et al. Immune dysregulation in human subjects with heterozygous germline mutations in CTLA4. Science. 2014;345:1623–7. doi: 10.1126/science. 1255904
188. Li G, Shi F, Liu J, Li Ye. The effect of CTLA-4 A49G polymorphism on rheumatoid arthritis risk: a meta-analysis. Diagn Pathol. 2014;9:157. doi: 10.1186/s13000-014-0157-0
189. Tsuboi H, Matsumoto I, Hagiwara S, et al. Efficacy and safety of abatacept for patients with Sjogren's syndrome associated with rheumatoid arthritis: rheumatoid arthritis with Orencia Trial toward Sjogren's syndrome Endocrinopathy (ROSE) trial – an open-label, one-year, prospective study – Interim analysis of 32 patients for 24 weeks. Mod Rheumatol. 2015;25:187–93. doi: 10.3190/14397595.2014.951144
190. Meiners PM, Vissink A, Kroese FGM, et al. Abatacept treatment reduces disease activity in early primary Sjogren's syndrome (open-label proof of concept ASAP study). Ann Rheum Dis. 2014 Jul;73(7):1393–6. doi: 10.1136/annrheumdis-2013- 204653
191. Payet J, Belkhir R, Gottenberg JE, et al. ACPA-positive primary Sjogren's syndrome: true primary or rheumatoid arthritis-associated Sjogren's syndrome? RMD Open. 2015;1:e000066. doi: 10.1136/rmdopen-2015-000066
192. Fuii W, Kohno M, Ishino H, et al. The rapid efficacy of abatacept in patients with rheumatoid vasculitis. Mod Rheumatol. 2012;22:630–4. doi: 10.3109/s10165-011-0559-8
193. Ostrowski RA, Tehrani R, Kadanoff R. Refractory adalt-onset Still disease sucessully treated with abatacept. J Clin Rheumatol. 2011;17:315–7. doi: 10.1097/RHU.0b013e31822c53ad
194. Quartuccio L, Maset M, de Vita S. Efficacy of abatacept in a refractory case of adult-oncet Still`s disease. Clin Exp Rheumatol. 2010;28:265–57.
195. Gardette A, Ottaviani S, Sellam J, et al. Does body mass index influence the response to abatacept in rheumatoid arthritis. Ann Rheum Dis. 2015;72(Suppl 4):1040–1. doi: 10.1136/annrhreumdis-eular.1258
196. Orban T, Bundy B, Becker DJ, et al. Co-stimulation modulation with abatacept in patients with recent oncet type 1 diabetes: a randomized, double-blind, placebo-controlled trial. Lancet. 2011;378:412–9. doi: 10.1016/S0140-6736(11)60886-6
197. Atzeni F, Sarzi-Puttini P, Mutti A, et al. Long-term safety in patients with rheumatoid arthritis. Autoimmun Rev. 2013;12:1115–7. doi: 10.1016/j.autrev.2013.06.011
198. Ramiro S, Gaujoux-Viala C, Nam JL, et al. Safety of synthetic and biological DMARDs: a systematic literature review informing the 2013 update of the EULAR recommendations for management of rheumatoid arthritis. Ann Rheum Dis. 2014;7:529–35. doi: 10.1136/annrheumdis-2013-204575
199. Simon TA, Askling J, Lacaille D, et al and the Abatacept Epidemiology Study Group. Infections requiring hospitalization in the abatacept clinical development program: an epidemiological assessment. Arthritis Res Ther. 2010;12:R67. doi: 10.1186/ar2984
200. Souto A, Maneiro JR, Sajgado E, et al. Risk of tuberculosis in patients with chronic immune-mediated inflammatory diseases treated with biologics and tofacitinid: a systemic review and meta-analysis of randomized controlled trials and long-term extension studies. Rheumatology. 2014;53:1872–85. doi: 10.1093/rheumatology/keu172
201. Motojima S, Nakashita T, Jibatake A, Ando K. Abatacept can be used safely for ra patients with interstitial lung disease. Arthritis Rheum. 2014;66(Suppl):472(abst).
202. Hirabara S, Kojima T, Takahashi N, et al. The safety and treatment efficacy of abatacept in rheumatoid arthritis patients with pulmonary complications: From the Tsurumai Biologics Communication Registry (TBCR) Multicenter Study. Arthritis Rheum. 2014;66 (Suppl):2(abst).
203. Nelson D, McLaughlin M, Ostor A. Abatacept and its impact on interstinal lung disease a systemic literature review. Ann Rheum Dis. 2015;74(Suppl 2):1015. doi: 10.1136/annrheumdis-2015-2004
204. Athanasakis K, Petrakis I, Kyriopoulos J. Investigating the value of abatacept in the treatment of rheumatoid arthritis: a systemic review of cost-effectiveness studies. ISRN Rheumatol. 2013 May 30;2013:256871. doi: 10.1155/2013/256871
Рецензия
Для цитирования:
Насонов Е.Л. Абатацепт при ревматоидном артрите: новая форма, новые механизмы, новые возможности. Научно-практическая ревматология. 2015;53(5):522-541. https://doi.org/10.14412/1995-4484-2015-522-541
For citation:
Nasonov E.L. ABATACEPT FOR RHEUMATOID ARTHRITIS: A NOVEL FORMULATION, NEW MECHANISMS, NEW POSSIBILITIES. Rheumatology Science and Practice. 2015;53(5):522-541. (In Russ.) https://doi.org/10.14412/1995-4484-2015-522-541
Просмотров:
1758
Послать статью по эл. почте 