Nevertheless, IL-25 was found to antagonize the pro-inflammatory effects of IL-17 A in both mouse models of collagen-induced arthritis (CIA), a mouse model for human RA, and experimental autoimmune encephalomyelitis (EAE), a mouse model for human multiple sclerosis (MS), thereby inhibiting the Th17 response and decreasing the degree of inflammation [9, 59, 60] (Table 1). This evidence concerns the gene IL25 and rheumatoid arthritis.