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The Journal of Immunology, 2006, 177: 566-573.
Copyright © 2006 by The American Association of Immunologists

IL-17 Plays an Important Role in the Development of Experimental Autoimmune Encephalomyelitis1

Yutaka Komiyama, Susumu Nakae2, Taizo Matsuki3, Aya Nambu, Harumichi Ishigame, Shigeru Kakuta, Katsuko Sudo4 and Yoichiro Iwakura5

Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan

IL-17 is a proinflammatory cytokine that activates T cells and other immune cells to produce a variety of cytokines, chemokines, and cell adhesion molecules. This cytokine is augmented in the sera and/or tissues of patients with contact dermatitis, asthma, and rheumatoid arthritis. We previously demonstrated that IL-17 is involved in the development of autoimmune arthritis and contact, delayed, and airway hypersensitivity in mice. As the expression of IL-17 is also augmented in multiple sclerosis, we examined the involvement of this cytokine in these diseases using IL-17–/– murine disease models. We found that the development of experimental autoimmune encephalomyelitis (EAE), the rodent model of multiple sclerosis, was significantly suppressed in IL-17–/– mice; these animals exhibited delayed onset, reduced maximum severity scores, ameliorated histological changes, and early recovery. T cell sensitization against myelin oligodendrocyte glycoprotein was reduced in IL-17–/– mice upon sensitization. The major producer of IL-17 upon treatment with myelin digodendrocyte glycopritein was CD4+ T cells rather than CD8+ T cells, and adoptive transfer of IL-17–/– CD4+ T cells inefficiently induced EAE in recipient mice. Notably, IL-17-producing T cells were increased in IFN-{gamma}–/– cells, while IFN-{gamma}-producing cells were increased in IL-17–/– cells, suggesting that IL-17 and IFN-{gamma} mutually regulate IFN-{gamma} and IL-17 production. These observations indicate that IL-17 rather than IFN-{gamma} plays a crucial role in the development of EAE.




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