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The pathogenetic mechanisms of reactive arthritis (ReA) are not fully understood. According to some studies, arthritis in ReA is a consequence of hyperproduction of pro-inflammatory cytokines, the results of others indicate that in ReA the Th1 immune response is reduced in favor of the Th2 immune response. The aim of our work was to study the levels of IL-17A and TNF-α in the blood serum of patients with ReA of various etiologies. The study revealed a significant increase in the content of IL-17A and TNF-α in patients with ReA compared with the control group. There were no significant differences in the cytokine profile of patients with ReA and infection-associated arthritis. The data obtained, in general, indicate the pro-inflammatory Th1 nature of the cytokine profile of the ReA patients examined by us and confirm the currently most common hypothesis of ReA pathogenesis, which is based on an imbalance of cytokines.
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