| pubmed-article:17289553 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17289553 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:17289553 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
| pubmed-article:17289553 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:17289553 | pubmed:dateCreated | 2007-2-9 | lld:pubmed |
| pubmed-article:17289553 | pubmed:abstractText | Recent studies demonstrated an IL-17-producer CD4+ T cell subpopulation, termed Th17, distinct from Th1 and Th2. It represents a different pro-inflammatory Th-cell lineage. This notion is supported by gene-targeted mice studies. Mice lacking IL-23 (p19-/-) do not develop experimental autoimmune encephalomyelitis (EAE) or collagen-induced arthritis (CIA), while knockout mice for the Th1 cytokine IL-12 (p35-/-) strongly develop both autoimmune diseases. Disease resistance by IL-23 knockout mice correlates well with the absence of IL-17-producing CD4(+) T lymphocytes in target organs despite normal presence of antigen-specific-IFN-gamma-producing Th1 cells. This finding may thus explain previous contradictory reports showing that anti-IFN-gamma-treated mice, IFN-gamma- or IFNR-deficient mice develop CIA or EAE. TGF-beta, IL-6 and IL-1 are the differentiation factors of Th17 cells. IL-23 is dispensable for this function, but necessary for Th17 expansion and survival. The master regulator that directs the differentiation program of Th17 cells is the orphan nuclear receptor RORgammat. IL-27, a member of the IL-12/IL-23 family, potently inhibits Th17 development. Evidence suggesting rheumatoid arthritis and multiple sclerosis as primarily IL-17 autoimmune inflammatory-mediated diseases is rapidly accumulating. The IL-17/23 axis of inflammation and related molecules may rise as therapeutic targets for treating these and perhaps other autoimmune diseases. | lld:pubmed |
| pubmed-article:17289553 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17289553 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17289553 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17289553 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17289553 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17289553 | pubmed:issn | 1568-9972 | lld:pubmed |
| pubmed-article:17289553 | pubmed:author | pubmed-author:CabralAntonio... | lld:pubmed |
| pubmed-article:17289553 | pubmed:author | pubmed-author:Furuzawa-Carb... | lld:pubmed |
| pubmed-article:17289553 | pubmed:author | pubmed-author:Vargas-RojasM... | lld:pubmed |
| pubmed-article:17289553 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17289553 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:17289553 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17289553 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17289553 | pubmed:pagination | 169-75 | lld:pubmed |
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| pubmed-article:17289553 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17289553 | pubmed:articleTitle | Autoimmune inflammation from the Th17 perspective. | lld:pubmed |
| pubmed-article:17289553 | pubmed:affiliation | Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga 15 Tlalpan, Mexico City 14000, Mexico. | lld:pubmed |
| pubmed-article:17289553 | pubmed:publicationType | Journal Article | lld:pubmed |
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