Source:http://linkedlifedata.com/resource/pubmed/id/16785554
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2006-6-20
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| pubmed:abstractText |
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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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, T-Lymphocyte,
http://linkedlifedata.com/resource/pubmed/chemical/Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/myelin oligodendrocyte...
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
177
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
566-73
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:16785554-Adoptive Transfer,
pubmed-meshheading:16785554-Amino Acid Sequence,
pubmed-meshheading:16785554-Animals,
pubmed-meshheading:16785554-Autoantibodies,
pubmed-meshheading:16785554-CD4-Positive T-Lymphocytes,
pubmed-meshheading:16785554-Cells, Cultured,
pubmed-meshheading:16785554-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:16785554-Epitopes, T-Lymphocyte,
pubmed-meshheading:16785554-Glycoproteins,
pubmed-meshheading:16785554-Interferon-gamma,
pubmed-meshheading:16785554-Interleukin-17,
pubmed-meshheading:16785554-Lymph Nodes,
pubmed-meshheading:16785554-Mice,
pubmed-meshheading:16785554-Mice, Inbred C57BL,
pubmed-meshheading:16785554-Mice, Knockout,
pubmed-meshheading:16785554-Molecular Sequence Data,
pubmed-meshheading:16785554-Peptide Fragments,
pubmed-meshheading:16785554-Up-Regulation
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| pubmed:year |
2006
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| pubmed:articleTitle |
IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis.
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| pubmed:affiliation |
Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
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| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|