Abstract
Deregulated production of interleukin-6 (IL-6) has been found in several chronic inflammatory autoimmune disorders, including rheumatoid arthritis (RA) and inflammatory bowel diseases. Treatment with tocilizumab, a humanized anti-human IL-6 receptor (IL-6R) antibody, significantly improved disease activity and inhibited the progression of joint destruction in RA patients, but the reason why IL-6 blockade causes improvement of RA is still unclear. In this review, we discuss the influence of anti-IL-6R antibody treatment on the differentiation of Th17 cells, which are thought to be involved in the pathogenesis of autoimmune diseases in animal models, present new results for the effect of anti-IL-6R antibody on the induction of Th17 cells in a mouse collagen-induced arthritis model, and come to the conclusion that anti-IL-6R antibody inhibited the differentiation of Th17 cells in mouse models. It is thought that this inhibitory action may contribute to the therapeutic effects of anti-IL-6R antibody in human autoimmune diseases.
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