| pubmed-article:19596803 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19596803 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
| pubmed-article:19596803 | lifeskim:mentions | umls-concept:C0085424 | lld:lifeskim |
| pubmed-article:19596803 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
| pubmed-article:19596803 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:19596803 | lifeskim:mentions | umls-concept:C1363844 | lld:lifeskim |
| pubmed-article:19596803 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:19596803 | pubmed:dateCreated | 2009-8-4 | lld:pubmed |
| pubmed-article:19596803 | pubmed:abstractText | We report that like other T cells cultured in the presence of transforming growth factor (TGF) beta, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-beta as well as purified ex vivo Th17 cells both produced IL-9. To determine if IL-9 has functional consequences in Th17-mediated inflammatory disease, we evaluated the role of IL-9 in the development and progression of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. The data show that IL-9 neutralization and IL-9 receptor deficiency attenuates disease, and this correlates with decreases in Th17 cells and IL-6-producing macrophages in the central nervous system, as well as mast cell numbers in the regional lymph nodes. Collectively, these data implicate IL-9 as a Th17-derived cytokine that can contribute to inflammatory disease. | lld:pubmed |
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| pubmed-article:19596803 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19596803 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19596803 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19596803 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:19596803 | pubmed:issn | 1540-9538 | lld:pubmed |
| pubmed-article:19596803 | pubmed:author | pubmed-author:NoelleRandolp... | lld:pubmed |
| pubmed-article:19596803 | pubmed:author | pubmed-author:WeaverCasey... | lld:pubmed |
| pubmed-article:19596803 | pubmed:author | pubmed-author:CoyleAnthony... | lld:pubmed |
| pubmed-article:19596803 | pubmed:author | pubmed-author:KasperLloyd... | lld:pubmed |
| pubmed-article:19596803 | pubmed:author | pubmed-author:SchreinerBett... | lld:pubmed |
| pubmed-article:19596803 | pubmed:author | pubmed-author:BecherBurkhar... | lld:pubmed |
| pubmed-article:19596803 | pubmed:author | pubmed-author:NowakElizabet... | lld:pubmed |
| pubmed-article:19596803 | pubmed:author | pubmed-author:TurnerHenriet... | lld:pubmed |
| pubmed-article:19596803 | pubmed:author | pubmed-author:Begum-HaqueSa... | lld:pubmed |
| pubmed-article:19596803 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19596803 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:19596803 | pubmed:volume | 206 | lld:pubmed |
| pubmed-article:19596803 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19596803 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19596803 | pubmed:pagination | 1653-60 | lld:pubmed |
| pubmed-article:19596803 | pubmed:dateRevised | 2010-9-24 | lld:pubmed |
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| pubmed-article:19596803 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19596803 | pubmed:articleTitle | IL-9 as a mediator of Th17-driven inflammatory disease. | lld:pubmed |
| pubmed-article:19596803 | pubmed:affiliation | Department of Microbiology and Immunology, Dartmouth Medical School and the Norris Cotton Cancer Center, Lebanon, NH 03756, USA. | lld:pubmed |
| pubmed-article:19596803 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19596803 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:19596803 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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