Epitopes described in "IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis."

Reference
Article Authors:Yutaka Komiyama; Susumu Nakae; Taizo Matsuki; Aya Nambu; Harumichi Ishigame; Shigeru Kakuta; Katsuko Sudo; Yoichiro Iwakura
Article Title:IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis.
Reference Detail
Reference ID:1005074
Abstract: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.
Affiliations:Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Date:2006
Reference Type:Literature
PubMed ID:16785554
Journal:J Immunol
Journal Volume:177
Article Pages:566-73
Journal ISSN:0022-1767
Article Chemical List:Autoantibodies;Epitopes, T-Lymphocyte;Glycoproteins;Interleukin-17;Myelin-Oligodendrocyte Glycoprotein;Peptide Fragments;myelin oligodendrocyte glycoprotein (35-55);Interferon-gamma
Article MeSH List:Adoptive Transfer; Amino Acid Sequence; Animals; Autoantibodies(biosynthesis); CD4-Positive T-Lymphocytes(immunology; metabolism; pathology; transplantation); Cells, Cultured; Encephalomyelitis, Autoimmune, Experimental(genetics; immunology; pathology; prevention & control); Epitopes, T-Lymphocyte(administration & dosage; immunology); Glycoproteins(administration & dosage; immunology); Interferon-gamma(biosynthesis; deficiency; genetics); Interleukin-17(biosynthesis; deficiency; genetics; physiology); Lymph Nodes(immunology; metabolism; pathology); Mice; Mice, Inbred C57BL; Mice, Knockout; Molecular Sequence Data; Myelin-Oligodendrocyte Glycoprotein; Peptide Fragments(administration & dosage; immunology); Up-Regulation(genetics; immunology)
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