| pubmed-article:16628262 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16628262 | lifeskim:mentions | umls-concept:C0014072 | lld:lifeskim |
| pubmed-article:16628262 | lifeskim:mentions | umls-concept:C0963088 | lld:lifeskim |
| pubmed-article:16628262 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:16628262 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:16628262 | pubmed:dateCreated | 2006-4-21 | lld:pubmed |
| pubmed-article:16628262 | pubmed:abstractText | Interleukin-23 (IL-23) is a heterodimeric cytokine that is composed of a p40 subunit, shared with the closely related cytokine IL-12, and a smaller IL-23p19 subunit. It belongs to a family of heterodimeric cytokines that also includes IL-12 and IL-27. Experimental autoimmune encephalomyelitis (EAE) is an autoimmune disease that serves as a model for multiple sclerosis, an inflammatory demyelinating disease of the central nervous system that is a frequent cause of disability in young adults. EAE is thought to be initiated by CD4+ T cells. The production of interferon-gamma and tumor necrosis factor-alpha (T helper 1 [Th1] phenotype) was considered a marker for the ability of such cells to induce disease. Consistent with this view, IL-12, a cytokine that induces the differentiation of Th1 cells, was considered essential for EAE susceptibility. However, it is now clear that IL-23 rather than IL-12 is required for EAE susceptibility. IL-23 induces a population of IL-17-producing cells that is more critically involved in EAE pathogenesis than Th1 cells. Here, we review the role of the IL-23 system in the pathophysiology of EAE. | lld:pubmed |
| pubmed-article:16628262 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16628262 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16628262 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16628262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16628262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16628262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16628262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16628262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16628262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16628262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16628262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16628262 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16628262 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:16628262 | pubmed:issn | 0214-0934 | lld:pubmed |
| pubmed-article:16628262 | pubmed:author | pubmed-author:RostamiA MAM | lld:pubmed |
| pubmed-article:16628262 | pubmed:author | pubmed-author:BarfH AHA | lld:pubmed |
| pubmed-article:16628262 | pubmed:author | pubmed-author:ZhangGuang-Xi... | lld:pubmed |
| pubmed-article:16628262 | pubmed:author | pubmed-author:GranBrunoB | lld:pubmed |
| pubmed-article:16628262 | pubmed:author | pubmed-author:FitzgeraldDen... | lld:pubmed |
| pubmed-article:16628262 | pubmed:copyrightInfo | Copyright 2006 Prous Science | lld:pubmed |
| pubmed-article:16628262 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16628262 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:16628262 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16628262 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16628262 | pubmed:pagination | 77-83 | lld:pubmed |
| pubmed-article:16628262 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:16628262 | pubmed:meshHeading | pubmed-meshheading:16628262... | lld:pubmed |
| pubmed-article:16628262 | pubmed:meshHeading | pubmed-meshheading:16628262... | lld:pubmed |
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| pubmed-article:16628262 | pubmed:meshHeading | pubmed-meshheading:16628262... | lld:pubmed |
| pubmed-article:16628262 | pubmed:meshHeading | pubmed-meshheading:16628262... | lld:pubmed |
| pubmed-article:16628262 | pubmed:meshHeading | pubmed-meshheading:16628262... | lld:pubmed |
| pubmed-article:16628262 | pubmed:meshHeading | pubmed-meshheading:16628262... | lld:pubmed |
| pubmed-article:16628262 | pubmed:meshHeading | pubmed-meshheading:16628262... | lld:pubmed |
| pubmed-article:16628262 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16628262 | pubmed:articleTitle | Pathophysiology of interleukin-23 in experimental autoimmune encephalomyelitis. | lld:pubmed |
| pubmed-article:16628262 | pubmed:affiliation | Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. | lld:pubmed |
| pubmed-article:16628262 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16628262 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:16628262 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16628262 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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