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No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis
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 univer...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Polish Society of Experimental and Clinical Immunology
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305616/ https://www.ncbi.nlm.nih.gov/pubmed/30588171 http://dx.doi.org/10.5114/ceji.2018.80045 |
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author | Sikorska, Dorota Rutkowski, Rafał Łuczak, Joanna Samborski, Włodzimierz Witowski, Janusz |
author_facet | Sikorska, Dorota Rutkowski, Rafał Łuczak, Joanna Samborski, Włodzimierz Witowski, Janusz |
author_sort | Sikorska, Dorota |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6305616 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Polish Society of Experimental and Clinical Immunology |
record_format | MEDLINE/PubMed |
spelling | pubmed-63056162018-12-26 No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis Sikorska, Dorota Rutkowski, Rafał Łuczak, Joanna Samborski, Włodzimierz Witowski, Janusz Cent Eur J Immunol Clinical Immunology 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. Polish Society of Experimental and Clinical Immunology 2018-10-30 2018 /pmc/articles/PMC6305616/ /pubmed/30588171 http://dx.doi.org/10.5114/ceji.2018.80045 Text en Copyright: © 2018 Polish Society of Experimental and Clinical Immunology http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license. |
spellingShingle | Clinical Immunology Sikorska, Dorota Rutkowski, Rafał Łuczak, Joanna Samborski, Włodzimierz Witowski, Janusz No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis |
title | No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis |
title_full | No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis |
title_fullStr | No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis |
title_full_unstemmed | No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis |
title_short | No effect of anti-TNF-α treatment on serum IL-17 in patients with rheumatoid arthritis |
title_sort | no effect of anti-tnf-α treatment on serum il-17 in patients with rheumatoid arthritis |
topic | Clinical Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305616/ https://www.ncbi.nlm.nih.gov/pubmed/30588171 http://dx.doi.org/10.5114/ceji.2018.80045 |
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