Studies using transgenic mice lacking either IL-17A or IL-17F showed that IL-17A plays a major role in the development of autoimmune diseases such as collagen-induced arthritis and Experimental Autoimmune Encephalitis (murine model of multiple sclerosis), and allergic diseases such as delayed-type hypersensitivity and contact hypersensitivity; in contrast, the role of IL-17F in these disease models was marginal (4, 5, 14, 33, 34). This evidence concerns the gene IL17A and multiple sclerosis.