pubmed-article:16906167 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16906167 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:16906167 | lifeskim:mentions | umls-concept:C0021764 | lld:lifeskim |
pubmed-article:16906167 | lifeskim:mentions | umls-concept:C1426048 | lld:lifeskim |
pubmed-article:16906167 | lifeskim:mentions | umls-concept:C0014072 | lld:lifeskim |
pubmed-article:16906167 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:16906167 | lifeskim:mentions | umls-concept:C2349209 | lld:lifeskim |
pubmed-article:16906167 | lifeskim:mentions | umls-concept:C1549649 | lld:lifeskim |
pubmed-article:16906167 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:16906167 | pubmed:dateCreated | 2006-8-22 | lld:pubmed |
pubmed-article:16906167 | pubmed:abstractText | Interleukin 27 (IL-27) was first characterized as a proinflammatory cytokine with T helper type 1-inducing activity. However, subsequent work has demonstrated that mice deficient in IL-27 receptor (IL-27R alpha) show exacerbated inflammatory responses to a variety of challenges, suggesting that IL-27 has important immunoregulatory functions in vivo. Here we demonstrate that IL-27R alpha-deficient mice were hypersusceptible to experimental autoimmune encephalomyelitis and generated more IL-17-producing T helper cells. IL-27 acted directly on effector T cells to suppress the development of IL-17-producing T helper cells mediated by IL-6 and transforming growth factor-beta. This suppressive activity was dependent on the transcription factor STAT1 and was independent of interferon-gamma. Finally, IL-27 suppressed IL-6-mediated T cell proliferation. These data provide a mechanistic explanation for the IL-27-mediated immune suppression noted in several in vivo models of inflammation. | lld:pubmed |
pubmed-article:16906167 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:language | eng | lld:pubmed |
pubmed-article:16906167 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906167 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16906167 | pubmed:month | Sep | lld:pubmed |
pubmed-article:16906167 | pubmed:issn | 1529-2908 | lld:pubmed |
pubmed-article:16906167 | pubmed:author | pubmed-author:BattenMarcelM | lld:pubmed |
pubmed-article:16906167 | pubmed:author | pubmed-author:LuJuJ | lld:pubmed |
pubmed-article:16906167 | pubmed:author | pubmed-author:GhilardiNicoN | lld:pubmed |
pubmed-article:16906167 | pubmed:author | pubmed-author:YiSothyS | lld:pubmed |
pubmed-article:16906167 | pubmed:author | pubmed-author:de... | lld:pubmed |
pubmed-article:16906167 | pubmed:author | pubmed-author:DanilenkoDimi... | lld:pubmed |
pubmed-article:16906167 | pubmed:author | pubmed-author:LeeJamesJ | lld:pubmed |
pubmed-article:16906167 | pubmed:author | pubmed-author:LucasSophieS | lld:pubmed |
pubmed-article:16906167 | pubmed:author | pubmed-author:KljavinNoelyn... | lld:pubmed |
pubmed-article:16906167 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16906167 | pubmed:volume | 7 | lld:pubmed |
pubmed-article:16906167 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16906167 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16906167 | pubmed:pagination | 929-36 | lld:pubmed |
pubmed-article:16906167 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:16906167 | pubmed:meshHeading | pubmed-meshheading:16906167... | lld:pubmed |
pubmed-article:16906167 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16906167 | pubmed:articleTitle | Interleukin 27 limits autoimmune encephalomyelitis by suppressing the development of interleukin 17-producing T cells. | lld:pubmed |
pubmed-article:16906167 | pubmed:affiliation | Department of Molecular Biology, Genentech, South San Francisco, California 94080, USA. | lld:pubmed |
pubmed-article:16906167 | pubmed:publicationType | Journal Article | lld:pubmed |
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