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The role of interleukin 1 in the development of human diseases

https://doi.org/10.14412/1995-4484-2018-19-27

Abstract

Human immuno-inflammatory diseases (IID), depending on the predominant mechanisms of immune activation, are divided into two main categories: autoimmune and autoinflammatory. It is assumed that hyperproduction of "proinflammatory" and immunoregulatory cytokine-interleukin 1 (IL 1) largely determines the "intersection" between the mechanisms underlying autoimmunity and autoinflammation in many IID. This review discusses the role of IL1 in the pathogenesis of IID, primarily those associated with the activation of NLRP3-inflammasome, and therapeutic perspectives of IL1β inhibition with monoclonal antibodies to IL1β – canakinumab. The study of the IL1 role in the regulation of interactions between innate (TLR activation, inflammasome) and adaptive (Th1 – and Th17-types of immune response) immunity and the efficacy of IL1 inhibitors may be important in terms of decoding the pathogenetic mechanisms of IID and the development of new approaches to personalized therapy.

About the Author

E. L. Nasonov
V.A. Nasonova Research Institute of Rheumatology; I.M. Sechenov First Moscow State Medical University (Sechenov University), Ministry of Health of Russia
Russian Federation

Department of Rheumatology, Institute of Professional Education, 34A, Kashirskoe Shosse, Moscow 115522;

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



References

1. McGonagle D, McDermott MF. A Proposed Classification of the Immunological Diseases. PLoS Med. 2006;3:e297. doi: 10.1371/journal.pmed.0030297

2. Doria A, Zen M, Bettio S, et al. Autoinflammation and autoimmunity: Bridging the divide. Autoimm Rev. 2012;12:22-30. doi: 10.1016/j.autrev.2012.07.018

3. Garlanda C, Dinarello CA, Mantovani A. The interleukin-1 family: back to the future. Immunity. 2013;39:1003-18. doi: 10.1016/j.immuni.2013.11.010

4. Dinarello CA. An expanding role for interleukin-1 blockade from gout to cancer. Molecular Med. 2014;20(Suppl 1):S43-S58. doi: 10.2119/molmed.2014.00232

5. Lopalco G, Cantarini L, Vitale A, et al. Interleukin-1 as a common denominator from autoinяammatory to autoimmune disorders: premises, perils, and perspectives. Mediat Inяamm. 2015;2015:194864.

6. Gabay G, Lamacchia C, Palme G. IL-1 pathways in inflammation and human diseases. Nat Rev Rheumatol. 2014;6:232-41. doi: 10.1038/nrrheum.2010.4

7. Sims JE, Smith DE. The IL-1 family: regulators of immunity. Nat Rev Immunol. 2010;10:89-102. doi: 10.1038/nri2691

8. Boraschi D, Italiani P, Weil S, Martin MU. The family of the interleukin-1 receptors. Immunol Rev. 2018;281(1):197-232. doi: 10.1111/imr.12606

9. Dinarello CA. Overview of the IL-1 family in innate inflammation and acquired immunity. Immunol Rev. 2018;281(1):8-27. doi: 10.1111/imr.12621

10. Schett G, Dayer J-M, Manger B. Interleukin-1 function and role in rheumatic disease. Nat Rev Rheumatol. 2016 Jan;12(1):14-24. doi: 10.1038/nrrheum.2016.166

11. Nasonov EL, Eliseev MS. Role of interleukin 1 in the development of human diseases. NauchnoPrakticheskaya Revmatologiya = Rheumatology Science and Practice. 2016;54(1):60-77 (In Russ.). doi: 10.14412/1995-4484-2016-60-77

12. 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

13. Nasonov EL. New possibilities of pharmacotherapy for immunoinflammatory rheumatic diseases: A focus on inhibitors of interleukin-17. NauchnoPrakticheskaya Revmatologiya = Rheumatology Science and Practice. 2017;55(1):68-86 (In Russ.). doi: 10.14412/1995-4484-2017-68-86

14. Spits H, Arti D, Colonna M, et al. Innate lymphoid cells – a proposal for uniform nomenclature. Nat Rev Immunol. 2013;13:145-9. doi: 10.1038/nri3365

15. Louati K, Berenbaum F. Fatigue in chronic inflammation – a link to pain pathways. Arthritis Res Ther. 2015 Oct 5;17:254. doi: 10.1186/s13075-015-0784-1

16. Roerink ME, van der Schaaf ME, Dinarello CA, et al. Interleukin-1 as a mediator of fatigue in disease: a narrative review. J Neuroinflammation. 2017;14(1):16. doi: 10.1186/s12974-017-0796-7

17. Jimenez-Dalmaroni MJ, Gerswhin ME, Adamopoulos IE. The critical role of Toll-like receptors – From microbial recognition to autoimmunity: A comprehensive review. Autoimmun Rev. 2016;15:1-8. doi: 10.1016/j.autrev.2015.08.009

18. Afonina IS, Mü ller C, Martin SJ, Beyaert R. Proteolytic processing of Interleukin-1 family cytokines: variations on a common theme. Immunity. 2015;42:991-1004. doi: 10.1016/j.immuni.2015.06.003

19. Broz P, Dixit VM. Inflammasomes: mechanism of assembly, regulation and signalling. Nat Rev Immunol. 2016;16:407-20. doi: 10.1038/nri.2016.58

20. Mangan MSJ, Olhava EJ, Roush WR, et al. Targeting the NLRP3 inflammasome in inflammatory diseases. Nat Rev Drug Discov. 2018;17(8):588-606. doi: 10.1038/nrd.2018.97

21. Netea MG, van de Veerdonk FL, van der Meer JW, et al. Inflammasome-independent regulation of IL-1-family cytokines. Annu Rev Immunol. 2015;33:49-77. doi: 10.1146/annurevimmunol-032414-112306

22. Schauer C, Janlo C, Munoz LE, et al. Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines. Nat Med. 2014;20:511-7. doi: 10.1038/nm.3547

23. Labrousse M, Kevorkian-Verguet C, Boursier G, et al. Mosaicism in autoinflammatory diseases: Cryopyrin-associated periodic syndromes (CAPS) and beyond. A systematic review. Crit Rev Clin Lab Sci. 2018 Sep;55(6):432-42. doi: 10.1080/10408363.2018.1488805

24. Harapas CR, Steiner A, Davidson S, Masters SL. An Update on Autoinflammatory Diseases: Inflammasomopathies. Curr Rheumatol Rep. 2018;20(7):40. doi: 10.1007/s11926-018-0750-y

25. Pardeo M, Bracaglia C, De Benedetti F. Systemic juvenile idiopathic arthritis: New insights into pathogenesis and cytokine directed therapies. Best Pract Res Clin Rheumatol. 2017;31(4):505- 16. doi: 10.1016/j.berh.2018.02.002

26. Cavalli G, Dinarello CA. Treating rheumatological diseases and co-morbidities with interleukin-1 blocking therapies. Rheumatology (Oxford). 2015;54:2134-44. doi: 10.1093/rheumatology/kev269

27. Gram H. Preclinical characterization and clinical development of ILARIS(®) (canakinumab) for the treatment of autoinflammatory diseases. Curr Opin Chem Biol. 2016;32:1-9. doi: 10.1016/j.cbpa.2015.12.003

28. Lonberg N. Human antibodies from transgenic animals. Nat Biotechnol. 2005;23:1117-25. doi: 10.1038/nbt1135

29. Fishwild DM, O'Donnell SL, Bengoechea T, et al. High-avidity human IgG kappa monoclonal antibodies from a novel strain of minilocus transgenic mice. Nat Biotechnol. 1996;14:845-51. doi: 10.1038/nbt0796-845

30. Alten R, Gram H, Joosten LA, et al. The human anti-IL-1 beta monoclonal antibody ACZ885 is effective in joint inflammation models in mice and in a proof-of-concept study in patients with rheumatoid arthritis. Arthritis Res Ther. 2008;10:R67. doi: 10.1186/ar2438

31. Rondeau JM, Ramage P, Zurini M, Gram H. The molecular mode of action and species specificity of canakinumab, a human monoclonal antibody neutralizing IL-1β. MAbs. 2015;7:1151-60. doi: 10.1080/19420862.2015.1081323

32. Wang D, Zhang S, Li L, et al. Structural insights into the assembly and activation of IL-1β with its receptors. Nat Immunol. 2010;11:905-11. doi: 10.1038/ni.1925

33. Thomas C, Bazan JF, Garcia KC. Structure of the activating IL-1 receptor signaling complex. Nat Struct Mol Biol. 2012;19:455-7. doi: 10.1038/nsmb.2260

34. Coleman KM, Gudjonsson JE, Stecher M. Open-Label Trial of MABp1, a True Human Monoclonal Antibody Targeting Interleukin 1β, for the Treatment of Psoriasis. JAMA Dermatol 2015;151:555-6. doi: 10.1001/jamadermatol.2014.5391

35. Shao B-Z, Xu Z-Q, Han B-Z, et al. NLRP3 inflammasome and its inhibitors: a review. Front Pharmacol. 2015;6:Article 262. doi: 10.3389/fpharm.2015.00262

36. Frenzel E, Wrenger S, Immenschuh S, et al. Acute-phase protein α1-antitrypsin--a novel regulator of angiopoietin-like protein 4 transcription and secretion. J Immunol. 2014;192:5354-62. doi: 10.4049/jimmunol.1400378

37. Joosten LA, Crisan TO, Azam T, et al. α-1-Anti-trypsin – Fc fusion protein ameliorates gouty arthritis by reducing release and extracellular processing of IL-1β and by the induction of endogenous IL-1Ra. Ann Rheum Dis. 2016;75:1219-27. doi: 10.1136/annrheumdis-2014-206966


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Nasonov E.L. The role of interleukin 1 in the development of human diseases. Rheumatology Science and Practice. 2018;56:19-27. (In Russ.) https://doi.org/10.14412/1995-4484-2018-19-27

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ISSN 1995-4484 (Print)
ISSN 1995-4492 (Online)