Abstract
Rheumatoid arthritis (RA) is one of the most common autoimmune disorders characterized by the chronic and progressive inflammation of various organs, most notably the synovia of joints leading to joint destruction, a shorter life expectancy, and reduced quality of life. Although we have substantial information about the pathophysiology of the disease with various groups of immune cells and soluble mediators identified to participate in the pathogenesis, several aspects of the altered immune functions and regulation in RA remain controversial. Animal models are especially useful in such scenarios. Recently research focused on IL-17 and IL-17 producing cells in various inflammatory diseases such as in RA and in different rodent models of RA. These studies provided occasionally contradictory results with IL-17 being more prominent in some of the models than in others; the findings of such experimental setups were sometimes inconclusive compared to the human data. The aim of this review is to summarize briefly the recent advancements on the role of IL-17, particularly in the different rodent models of RA.
Highlights
Rheumatoid arthritis (RA) is a systemic autoimmune disorder characterized by chronic synovitis leading to the progressive destruction of joints accompanied by systemic inflammation and the production of autoantibodies [1]
There are many animal models of RA, which might represent the heterogeneity of the human disease itself
Based on the studies available, the autoimmune arthritis observed in SKG, K/BxN serum transfer, and Collagen-Induced Arthritis (CIA) models might be clearly IL-17-dependent disease
Summary
Rheumatoid arthritis (RA) is a systemic autoimmune disorder characterized by chronic synovitis leading to the progressive destruction of joints accompanied by systemic inflammation and the production of autoantibodies [1]. Little is known about how and when the disease starts the new therapeutic agents proved to be much more effective than the conventional drugs used earlier. These diseasemodifying antirheumatic drugs (DMARDs) do not alter the autoimmunity per se; they do not lead to remission in all of the patients. The central role of TNFα in the inflammatory phase of RA has been described earlier, but with the description of Th17 cells and the involvement of IL-17 in RA some new potential treatment options became available only recently [3]. Our review will mainly focus on the role of IL-17 in RA, the rodent models of the disease, which all contributed to the development of novel therapeutic agents
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