eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
Current issue Archive Manuscripts accepted About the journal Abstracting and indexing Subscription Contact Instructions for authors
SCImago Journal & Country Rank

3/2018
vol. 43
 
Share:
Share:
more
 
 
abstract:
Clinical immunology

No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis

Dorota Sikorska, Rafał Rutkowski, Joanna Łuczak, Włodzimierz Samborski, Janusz Witowski

(Centr Eur J Immunol 2018; 43 (3): 270-275)
Online publish date: 2018/10/30
View full text
Get citation
ENW
EndNote
BIB
JabRef, Mendeley
RIS
Papers, Reference Manager, RefWorks, Zotero
AMA
APA
Chicago
Harvard
MLA
Vancouver
 
Introduction
Interleukin 17 (IL-17) and CC-chemokine ligand 20 (CCL20) are increasingly implicated in the pathogenesis of rheumatoid arthritis (RA). A correlation has been reported to exist between serum levels of IL-17 and CCL20 and the disease activity. However, such an effect has not been universally demonstrated. The aim of the present study was to investigate if serum levels of IL-17 and/or CCL20 reflect the disease activity and response to anti-TNF-α therapy in patients with RA.

Material and methods
Twenty-two RA patients qualified to receive anti-TNF-α treatment were prospectively assessed before and after 12 weeks of therapy. Serum concentrations of IL-17 and CCL20 were measured with high-sensitivity immunoassays. Disease activity was assessed by the 28-joint disease activity score (DAS28).

Results
Twelve weeks of therapy resulted in a satisfactory therapeutic response in the majority (91%) of patients (reflected both by clinical and standard biochemical criteria). However, serum concentrations of IL-17 and CCL20 did not change significantly over the course of therapy Moreover, they did not correlate with the disease activity, patient characteristics, and their response to therapy.

Conclusions
Serum levels of IL-17 and CCL20 do not reflect changes in the clinical and biochemical status that occur in patients undergoing anti-TNF-α treatment for RA. The lack of such an association indicates that IL-17 signalling is not affected by anti-TNF-α therapy and is thus not critically involved in the disease pathogenesis.

keywords:

rheumatoid arthritis, interleukin-17, chemokine CCL20, anti-TNF-α treatment

references:
Furst DE, Emery P (2014): Rheumatoid arthritis pathophysiology: update on emerging cytokine and cytokine-associated cell targets. Rheumatology (Oxford) 53: 1560-1569.
Low AS, Symmons DP, Lunt M, et al. (2017): Relationship between exposure to tumour necrosis factor inhibitor therapy and incidence and severity of myocardial infarction in patients with rheumatoid arthritis. Ann Rheum Dis 76: 654-660.
Mewar D, Wilson AG (2011): Treatment of rheumatoid arthritis with tumour necrosis factor inhibitors. Br J Pharmacol 162: 785-791.
Eder P, Linke K, Witowski J (2016): Update on the mechanisms of action of antiTNF-αlpha antibodies and their clinical implications in inflammatory bowel disease. Pol Arch Med Wewn 126: 772-780.
Ohshima S, Saeki Y, Mima T, et al. (1999): Long-term follow-up of the changes in circulating cytokines, soluble cytokine receptors, and white blood cell subset counts in patients with rheumatoid arthritis (RA) after monoclonal anti-TNF alpha antibody therapy. J Clin Immunol 19: 305-313.
Barrera P, Joosten LA, den Broeder AA, et al. (2001): Effects of treatment with a fully human anti-tumour necrosis factor alpha monoclonal antibody on the local and systemic homeostasis of interleukin 1 and TNFαlpha in patients with rheumatoid arthritis. Ann Rheum Dis 60: 660-669.
Sadik CD, Kim ND, Alekseeva E, Luster AD (2011). IL-17RA signaling amplifies antibody-induced arthritis. PloS One 6: e26342.
Kugyelka R, Kohl Z, Olasz K, et al. (2016): Enigma of IL-17 and Th17 Cells in Rheumatoid Arthritis and in Autoimmune Animal Models of Arthritis. Mediators Inflamm 2016: 6145810.
Lubberts E (2015): The IL-23-IL-17 axis in inflammatory arthritis. Nat Rev Rheumatol 11: 415-429.
Shahrara S, Pickens SR, Mandelin AM, 2nd, et al. (2010): IL-17-mediated monocyte migration occurs partially through CC chemokine ligand 2/monocyte chemoattractant protein-1 induction. J Immunol 184: 4479-4487.
Acosta-Rodriguez EV, Napolitani G, Lanzavecchia A, Sallusto F (2007): Interleukins 1beta and 6 but not transforming growth factor-beta are essential for the differentiation of interleukin 17-producing human T helper cells. Nat Immunol 8: 942-949.
Alzabin S, Abraham SM, Taher TE, et al. (2012): Incomplete response of inflammatory arthritis to TNFαlpha blockade is associated with the Th17 pathway. Ann Rheum Dis 71: 1741-1748.
Chen DY, Chen YM, Chen HH, et al. (2011): Increasing levels of circulating Th17 cells and interleukin-17 in rheumatoid arthritis patients with an inadequate response to anti-TNF-αlpha therapy. Arthritis Res Ther 13: R126.
Rosu A, Margaritescu C, Stepan A (2012): IL-17 patterns in synovium, serum and synovial fluid from treatment-naive, early rheumatoid arthritis patients. Rom J Morphol Embryol 53: 73-80.
Zhao PW, Jiang WG, Wang L, et al. (2014): Plasma levels of IL-37 and correlation with TNF-αlpha, IL-17A, and disease activity during DMARD treatment of rheumatoid arthritis. PloS One 9: e95346.
Metawi SA, Abbas D, Kamal MM, Ibrahim MK (2011): Serum and synovial fluid levels of interleukin-17 in correlation with disease activity in patients with RA. Clin Rheumatol 30: 1201-1207.
Kawashiri SY, Kawakami A, Iwamoto N, et al. (2009): Proinflammatory cytokines synergistically enhance the production of chemokine ligand 20 (CCL20) from rheumatoid fibroblast-like synovial cells in vitro and serum CCL20 is reduced in vivo by biologic disease-modifying antirheumatic drugs. J Rheumatol 36: 2397-2402.
Kageyama Y, Kobayashi H, Kato N (2009): Infliximab treatment reduces the serum levels of interleukin-23 in patients with rheumatoid arthritis. Mod Rheumatol 19: 657-662.
Rasmussen TK, Andersen T, Hvid M, et al. (2010): Increased interleukin 21 (IL-21) and IL-23 are associated with increased disease activity and with radiographic status in patients with early rheumatoid arthritis. J Rheumatol 37: 2014-2020.
Walters HM, Pan N, Lehman TJ, et al. (2016): The impact of disease activity and tumour necrosis factor-alpha inhibitor therapy on cytokine levels in juvenile idiopathic arthritis. Clin Exp Immunol 184: 308-317.
Nirula A, Nilsen J, Klekotka P, et al. (2016): Effect of IL-17 receptor A blockade with brodalumab in inflammatory diseases. Rheumatology (Oxford) 55 (Suppl 2): ii43-ii55.
Kunwar S, Dahal K, Sharma S (2016): Anti-IL-17 therapy in treatment of rheumatoid arthritis: a systematic literature review and meta-analysis of randomized controlled trials. Rheumatol Int 36: 1065-1075.
Raza K, Falciani F, Curnow SJ, et al. (2005): Early rheumatoid arthritis is characterized by a distinct and transient synovial fluid cytokine profile of T cell and stromal cell origin. Arthritis Res Ther 7: R784-795.
Aletaha D, Neogi T, Silman AJ, et al. (2010): 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis 69: 1580-1588.
Prevoo ML, van ‘t Hof MA, Kuper HH, et al. (1995): Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum 38: 44-48.
van Gestel AM, Prevoo ML, van ‘t Hof MA, et al. (1996): Development and validation of the European League Against Rheumatism response criteria for rheumatoid arthritis. Comparison with the preliminary American College of Rheumatology and the World Health Organization/International League Against Rheumatism Criteria. Arthritis Rheum 39: 34-40.
Izumi K, Kaneko Y, Hashizume M, et al. (2015): Baseline Serum Osteopontin Levels Predict the Clinical Effectiveness of Tocilizumab but Not Infliximab in Biologic-Naive Patients with Rheumatoid Arthritis: A Single-Center Prospective Study at 1 Year (the Keio First-Bio Cohort Study). PloS One 10: e0145468.
Avdeev AS, Novikov AA, Aleksandrova EN, et al. (2014): [The importance of cytokine profile characteristics for evaluating the therapeutic effectiveness of monoclonal antibodies against IL-6 receptors in patients with rheumatoid arthritis]. Klin Med (Mosk) 92: 28-34.
Yue C, You X, Zhao L, et al. (2010): The effects of adalimumab and methotrexate treatment on peripheral Th17 cells and IL-17/IL-6 secretion in rheumatoid arthritis patients. Rheumatol Int 30: 1553-1557.
Yamada H, Nakashima Y, Okazaki K, et al. (2008): Th1 but not Th17 cells predominate in the joints of patients with rheumatoid arthritis. Ann Rheum Dis 67: 1299-1304.
Cornelissen F, Asmawidjaja PS, Mus AM, et al. (2013): IL-23 dependent and independent stages of experimental arthritis: no clinical effect of therapeutic IL-23p19 inhibition in collagen-induced arthritis. PloS One 8: e57553.
Jain M, Attur M, Furer V, et al. (2015): Increased plasma IL-17F levels in rheumatoid arthritis patients are responsive to methotrexate, anti-TNF, and T cell costimulatory modulation. Inflammation 38: 180-186.
Gaffen SL (2009): Structure and signalling in the IL-17 receptor family. Nat Rev Immunol 9: 556-567.
Koenders MI, Lubberts E, Oppers-Walgreen B, et al. (2005): Blocking of interleukin-17 during reactivation of experimental arthritis prevents joint inflammation and bone erosion by decreasing RANKL and interleukin-1. Am J Pathol 167: 141-149.
Kochi Y, Okada Y, Suzuki A, et al. (2010): A regulatory variant in CCR6 is associated with rheumatoid arthritis susceptibility. Nat Genet 42: 515-519.
Andersson KM, Cavallini NF, Hu D, et al. (2015): Pathogenic Transdifferentiation of Th17 Cells Contribute to Perpetuation of Rheumatoid Arthritis during Anti-TNF Treatment. Mol Med 21: 536-543.
Balato A, Scala E, Balato N, et al. (2017): Biologics that inhibit the Th17 pathway and related cytokines to treat inflammatory disorders. Expert Opin Biol Ther 17: 1363-1374.
Johnston A, Guzman AM, Swindell WR, et al. (2014): Early tissue responses in psoriasis to the antitumour necrosis factor-alpha biologic etanercept suggest reduced interleukin-17 receptor expression and signalling. Br J Dermatol 171: 97-107.
Aerts NE, De Knop KJ, Leysen J, et al. (2010): Increased IL-17 production by peripheral T helper cells after tumour necrosis factor blockade in rheumatoid arthritis is accompanied by inhibition of migration-associated chemokine receptor expression.
FEATURED PRODUCTS
Quick links
© 2018 Termedia Sp. z o.o. All rights reserved.
Developed by Bentus.
PayU - płatności internetowe