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[dignan]

Looks as though we all owe interferon-gamma a bit of an apology...and IL-17 is coming right off my Christmas card list...



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

J Immunol. 2006 Jul 1;177(1):566-73.
Komiyama Y, Nakae S, Matsuki T, Nambu A, Ishigame H, Kakuta S, Sudo K, Iwakura Y.
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.

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum