Preview

Rheumatology Science and Practice

Advanced search

PROSPECTS FOR USING INTERLEUKIN-17 INHIBITORS, A NEW CLASS OF DRUGS FOR TARGETED THERAPY OF PSORIATIC ARTHRITIS

https://doi.org/10.14412/1995-4484-2016-346-351

Abstract

The paradigm of therapy for psoriatic arthritis (PsA) has recently undergone considerable changes due to development and clinical introduction of highly effective targeted drugs based on monoclonal antibodies – inhibitors of different cytokines. The data available in the literature on the possibilities of using interleukin 17 (IL-17) inhibitors as a promising PsA therapy were analyzed. The IL-17-mediated signaling pathway was shown to play an important role in both the chronization of synovial inflammation and in the occurrence and development of bone erosions, bone proliferation, and enthesitis in this disease. The combination of the high efficiency and acceptable safety of IL-17 and IL-23 inhibitors could suggest that they might be used as first-line agents for the treatment of PsA or as second-line therapy if tumor necrosis factor-α inhibitors were ineffective or intolerable. The active design of three novel drugs aimed at suppressing IL-17 was noted to only confirm the key role of this cytokine in developing psoriatic disease.

The paper gives the data of clinical trials supporting the high efficacy of secukinumab against the key clinical manifestations of PsA. The most important advantage of the drug is the lack of immunogenicity. It is pointed out that the latest edition of the EULAR Guidelines (2015) proposes to include this class of drugs in an algorithm for the treatment of PsA patients.

About the Author

T. V. Korotaeva
V.A. Nasonova Research Institute of Rheumatology
Russian Federation
34A, Kashirskoe Shosse, Moscow 115522


References

1. Smolen JS, Braun J, Dougados M, et al. Treating spondyloarthritis, including ankylosing spondylitis and psoriatic arthritis, to target: recommendations of an international task force. Ann Rheum Dis. 2014;73:6-16. doi: 10.1136/annrheumdis-2013-203419

2. Coates LC, Moverly AR, McParland L, et al. Effect of tight control of inflammation in early psoriatic arthritis (TICOPA): a UK multicentre, open-label, randomized controlled trial. Lancet. 2015;386(10012):2489-98. doi: 10.1016/s0140-6736(15)00347-5

3. Kavanaugh A, McInnes I, Mease P, et al. Golimumab, a new human tumor necrosis factor alpha antibody, administered every four weeks as a subcutaneous injection in psoriatic arthritis: twenty-four-week eficacy and safety results of a randomized, placebocontrolled study. Arthritis Rheum. 2009;60(4):976-86. doi: 10.1002/art.24403

4. McInnes I, Kavanaugh A, Gottlieb A, et al. Efficacy and safety of ustekinumab in patients with active psoriatic arthritis: 1 year results of the phase 3, multicentre, double-blind, placebo-controlled PSUMMIT 1 trial. Lancet. 2013;382(9894):780-9. doi: 10.1016/S0140-6736(13)60594-2

5. Vogelzang EH, Kneepkens EL, Nurmohamed MT, et al. Antiadalimumab antibodies and adalimumab concentrations in psoriatic arthritis; an association with disease activity at 28 and 52 weeks of follow-up. Ann Rheum Dis. 2014;73:2178-2182. doi: 10.1136/annrheumdis-2014-205554

6. Glintborg B, Ostergaard M, Dreyer L, et al. Treatment response, drug survival, and predictors thereof in 764 patients with psoriatic arthritis treated with anti-tumor necrosis factor alpha therapy: results from the nationwide Danish DANBIO registry. Arthritis Rheum. 2011;63:382-90. doi: 10.1002/art.30117

7. Finzel S, Kraus S, Schmidt S, et al. Bone anabolic changes progress in psoriatic arthritis patients despite treatment with methotrexate or tumour necrosis factor inhibitors. Ann Rheum Dis. 2012;72(7):1176-81. doi: 10.1136/annrheumdis-2012-20158

8. Menon B, Gullick NJ, Walter GJ, et al. Interleukin-17+CD8+ T cells are enriched in the joints of patients with psoriatic arthritis and correlate with disease activity and joint damage progression. Arthritis Rheum. 2014;66:1272-81. doi: 10.1002/art.38376

9. Miossec P, Kolls JK. Targeting IL-17 and Th17 cells in chronic inflammation. Nat Rev Drug Discov. 2012;11(10):763-76. doi: 10.1038/nrd3794

10. Raychaudhuri SK, Saxena A, Raychaudhuri SP. Role of IL-17 in the pathogenesis of psoriatic arthritis and axial spondyloarthritis. Clin Rheumatol. 2015;34(6):1019-23. doi: 10.1007/s10067-015-2961-7

11. Rouvier E, Luciani MF, Mattei MG, et al. CTLA-8, cloned from an activated T cell, bearing AU-rich messenger RNA instability sequences, and homologous to a herpesvirus saimiri gene. J Immunol. 1993;150:5445-56.

12. Van den Berg WB, McInnes IB. Th17 cells and IL-17 a-focus on immunopathogenesis and immunotherapeutics. Semin Arthritis Rheum. 2013;43:158-70. doi: 10.1016/j.semarthrit.2013.04.006

13. Miossec P, Korn T, Kuchroo VK. Interleukin-17 and type 17 helper T cells. N Engl J Med. 2009;361:888-98. doi: 10.1056/NEJMra0707449

14. Frleta M, Siebert S, McInnes IB. The interleukin-17 pathway in psoriasis and psoriatic arthritis: disease pathogenesis and possibilities of treatment. Curr Rheumatol Rep. 2014;16:414. doi: 10.1007/s11926-014-0414-y

15. Johansen C, Usher PA, Kjellerup RB, et al. Characterization of the interleukin-17 isoform and receptors in lesional psoriatic skin. Br J Dermatol. 2009;160(2):319-24. doi: 10.1111/j.1365-2133.2008.08902.x

16. Jandus C, Bioley G, Rivas JP, et al. Increased numbers of circulating polyfunctional Th17 memory cells in patients with seronegative spondylarthritides. Arthritis Rheum. 2008;58:2307-17. doi: 10.1002/art.23655

17. Kagami S, Rizzo HL, Lee JJ, et al. Circulating Th17, Th22, and Th1 cells are increased in psoriasis. J Invest Dermatol. 2010;130:1373-83. doi: 10.1038/jid.2009.399

18. Lin AM, Rubin CJ, Khandpur R, et al. Mast cells and neutrophils release IL-17 through extracellular trap formation in psoriasis. J Immunol. 2011;187:490-500. doi: 10.4049/jimmunol.1100123

19. Noordenbos T, Yeremenko N, Gofita I, et al. Interleukin-17-positive mast cells contribute to synovial inflammation in spondylarthritis. Arthritis Rheum. 2012;64:99-109. doi: 10.1002/art.33396

20. Lubberts E, Koenders MI, Oppers-Walgreen B, et al. Treatment with a neutralizing anti-murine interleukin-17 antibody after the onset of collagen-induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion. Arthritis Rheum. 2004;50:650-9. doi: 10.1002/art.20001

21. Pllinger B, Junt T, Metzler B, et al. Th17 cells, not IL-17+ γδ T cells, drive arthritic bone destruction in mice and humans. J Immunol. 2011;186:2602-12. doi: 10.4049/jimmunol.1003370

22. Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361:496-509. doi: 10.1056/NEJMra0804595

23. Raychaudhuri SP. Role of IL-17 in psoriasis and psoriatic arthritis. Clin Rev Allergy Immunol. 2013;44:183-93. doi: 10.1007/s12016-012-8307-1

24. Suzuki E, Mellins ED, Gershwin ME, et al. The IL-23/IL-17 axis in psoriatic arthritis. Autoimmun Rev. 2014;13(4-5):496-502. doi: 10.1016/j.autrev.2014.01.050

25. Annunziato F, Cosmi L, Santarlasci V, et al. Phenotypic and functional features of human Th17 cells. J Exp Med. 2007 Aug 6;204(8):1849-61. doi.org/10.1084/jem.20070663

26. Gaffen SL. The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing. Nat Rev Immunol. 2014 Sep;14(9):585-600. doi: 10.1038/nri3707

27. Langley RG, Elewski BE, Lebwohl M, et al. Secukinumab in plaque psoriasis – results of two phase 3 trials. N Engl J Med. 2014;371:326-38. doi: 10.1056/NEJMoa1314258. Epub 2014 Jul 9.

28. McInnes IB, Mease PJ, Kirkham B, et al; on behalf of the FUTURE 2 Study Group. Secukinumab, a human anti-interleukin-17A monoclonal antibody, in patients with monoclonal antibody, in patients with psoriatic arthritis (FUTURE 2): a randomised, double-blinded, placebo-controlled, phase 3 trial. Lancet. 2015 Sep 19;386(9999):1137-46. doi: 10.1016/S0140-6736(15)61134-5

29. Van der Heijde D, Aletaha D, Carmona L, et al. 2014 Update of the EULAR standardized operating procedures for EULARendorsed recommendations. Ann Rheum Dis. 2015 Jan;74(1):8-13. doi: 10.1136/annrheumdis-2014-206350

30. Ritchlin C, Rahman P, Kavanaugh A, et al. Efficacy and safety of the anti-IL-12/23 p40 monoclonal antibody, ustekinumab, in patients with active psoriatic arthritis despite conventional nonbiological and biological anti-tumour necrosis factor therapy: 6-month and 1-year results of the phase 3, multicentre, doubleblind, placebo-controlled, randomized PSUMMIT 2 trial. Ann Rheum Dis. 2014;73:990-9. doi: 10.1136/annrheumdis-2013-204655

31. McInnes IB, Sieper J, Braun J, et al. Efficacy and safety of secukinumab, a fully human anti-interleukin-17A monoclonal antibody, in patients with moderate-to severe psoriatic arthritis: a 24-week, randomised, double-blind, placebo-controlled, phase II proof-ofconcept trial. Ann Rheum Dis. 2014;73:349-56. doi: 10.1136/annrheumdis-2012-202646. Epub 2013 Jan 29.

32. Griffiths CE, Reich K, Lebwohl M, et al. Comparison of ixekizumab with etanercept or placebo in moderate-to-severe psoriasis (UNCOVER-2 and UNCOVER-3): results from two phase 3 randomised trials. Lancet. 2015;386(9993):541-51. doi: 10.1016/S0140-6736(15)60125-8

33. Han C, Robinson DW, Hackett MV, et al. Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. J Rheumatol. 2006;33:2167-72.

34. Gladman DD, Ang M, Su L, et al. Cardiovascular morbidity in psoriatic arthritis. Ann Rheum Dis. 2009;68:1131-5. doi: 10.1136/ard.2008.094839

35. Husted JA, Thavaneswaran A, Chandran V, et al. Cardiovascular and other comorbidities in patients with psoriatic arthritis: a comparison with patients with psoriasis. Arthritis Care Res (Hoboken). 2011;63:1729-35. doi: 10.1002/acr.20627

36. Mease PJ, McInnes IB, Kirkham B, et al. Secukinumab inhibition of interleukin-17A in patients with psoriatic arthritis. N Engl J Med. 2015;373:1329-39. doi: 10.1056/NEJMoa1412679

37. Leonardi C, Matheson R, Zachariae C, et al. Antiinterleukin-17 monoclonal antibody ixekizumab in chronic plaque psoriasis. N Engl J Med. 2012;366:1190-9. doi: 10.1056/NEJMoa1109997

38. Papp KA, Leonardi C, Menter A, et al. Brodalumab, an antiinterleukin-17-receptor antibody for psoriasis. N Engl J Med. 2012;366:1181-9. doi: 10.1056/NEJMoa1109017

39. Mease PJ, et al. A randomized, double-blind, active- and placebocontrolled phase 3 study of efficacy and safety of ixekizumab, adalimumab, and placebo therapy in patients naive to biologic disease modifying anti-rheumatic drugs with active psoriatic arthritis 2015 ACR/ARHP Annual Meeting. Abstract number 977 Date of first publication: September 29, 2015.

40. Glintborg B, Ostergaard M, Krogh NS, et al. Clinical response, drug survival, and predictors thereof among 548 patients with psoriatic arthritis who switched tumor necrosis factor α inhibitor therapy: results from the Danish Nationwide DANBIO Registry. Arthritis Rheum. 2013;65:1213-23. doi: 10.1002/art.37876

41. Kavanaugh A, Krueger GG, Beutler A, et al. Infliximab maintains a high degree of clinical response in patients with active psoriatic arthritis through 1 year of treatment: results from the IMPACT 2 trial. Ann Rheum Dis. 2007;66:498-505. doi: 10.1136/ard.2006.058339

42. Fagerli KM, Lie E, van der Heijde D, et al. Switching between TNF inhibitors in psoriatic arthritis: data from the NOR-DMARD study. Ann Rheum Dis. 2013;72:1840-4. doi: 10.1136/annrheumdis-2012-203018

43. Gossec L, Smolen J, Ramiro S. European League Against Rheumatism (EULAR) recommendations for the management of psoriatic arthritis with pharmacological therapies: 2015 update. Ann Rheum Dis. 2015;0:1-12. doi: 10.1136/annrheumdis-2015-208337


Review

For citations:


Korotaeva T.V. PROSPECTS FOR USING INTERLEUKIN-17 INHIBITORS, A NEW CLASS OF DRUGS FOR TARGETED THERAPY OF PSORIATIC ARTHRITIS. Rheumatology Science and Practice. 2016;54(3):346-351. (In Russ.) https://doi.org/10.14412/1995-4484-2016-346-351

Views: 1057


Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.


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