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3/2018
vol. 43
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
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
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