CLINICAL IMMUNOLOGY
No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis
Submission date: 2017-10-12
Final revision date: 2017-11-11
Acceptance date: 2017-11-14
Publication date: 2018-10-30
Cent Eur J Immunol 2018;43(3):270-275
KEYWORDS
ABSTRACT
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.
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.
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