INVESTIGATION OF CYTOKINE PROFILE IN PATIENTS WITH REACTIVE ARTHRITIS

Pathogenesis of reactive arthritis (ReA) is not clear yet. Several trials suggest that increased production of proinflammatory cytokines is responsible for development of arthritis in ReA, while other studies report that Th1 cytokine response in ReA is impaired in favor of Th2 response. The aim of o...

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Published in:	Medit͡s︡inskai͡a︡ immunologii͡a Vol. 10; no. 2-3; pp. 167 - 172
Main Authors:	Gaponova, T. V., Lila, A. M., Shemerovskaya, T. G., Zakharova, G. A., Maslyaeva, T. N.
Format:	Journal Article
Language:	English
Published:	St. Petersburg branch of the Russian Association of Allergologists and Clinical Immunologists 16-07-2014
Subjects:	cytokines ifnγ il-1ra il-1β il-4 il-6 infection reactive arthritis tnfα
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Summary:	Pathogenesis of reactive arthritis (ReA) is not clear yet. Several trials suggest that increased production of proinflammatory cytokines is responsible for development of arthritis in ReA, while other studies report that Th1 cytokine response in ReA is impaired in favor of Th2 response. The aim of our study was to investigate serum levels of cytokines IL-1β, IL-4, IL-6, TNFα, IFNγ and IL-1Ra in the patients with ReA of different etiology, as compared with infection-related arthritis. The results of our study had demonstrated that serum levels of IL-1β and TNFα in the patients with ReA were significantly higher, whereas IL-1Ra, IL-4, IL-6 proved to be significantly lower than in healthy controls. Serum levels of IL-6 were significantly higher in patients with chronic ReA, as compared to the cases of acute and recurrent ReA. No significant differences in cytokine profiles were found between the patients with ReA, and the persons with infection-related arthritis. The data obtained are, generally, suggestive for proinflammatory Th1 cytokine profile in ReA patients studied, this confirming the mostly assumed pathogenetic hypothesis for reactive arthritis where an underlying cytokine imbalance is suggested. (Med. Immunol., 2008, vol. 10, N 2-3, pp 167-172).
ISSN:	1563-0625 2313-741X
DOI:	10.15789/1563-0625-2008-2-3-167-172