| pubmed-article:18571443 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18571443 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
| pubmed-article:18571443 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:18571443 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
| pubmed-article:18571443 | lifeskim:mentions | umls-concept:C1420806 | lld:lifeskim |
| pubmed-article:18571443 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:18571443 | lifeskim:mentions | umls-concept:C1880371 | lld:lifeskim |
| pubmed-article:18571443 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18571443 | pubmed:dateCreated | 2008-7-17 | lld:pubmed |
| pubmed-article:18571443 | pubmed:abstractText | DR3 (TRAMP, LARD, WSL-1, TNFRSF25) is a death-domain-containing tumor necrosis factor (TNF)-family receptor primarily expressed on T cells. TL1A, the TNF-family ligand for DR3, can costimulate T cells, but the physiological function of TL1A-DR3 interactions in immune responses is not known. Using DR3-deficient mice, we identified DR3 as the receptor responsible for TL1A-induced T cell costimulation and dendritic cells as the likely source for TL1A during T cell activation. Despite its role in costimulation, DR3 was not required for in vivo T cell priming, for polarization into T helper 1 (Th1), Th2, or Th17 effector cell subtypes, or for effective control of infection with Toxoplasma gondii. Instead, DR3 expression was required on T cells for immunopathology, local T cell accumulation, and cytokine production in Experimental Autoimmune Encephalomyelitis (EAE) and allergic lung inflammation, disease models that depend on distinct effector T cell subsets. DR3 could be an attractive therapeutic target for T cell-mediated autoimmune and allergic diseases. | lld:pubmed |
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| pubmed-article:18571443 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18571443 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18571443 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18571443 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:18571443 | pubmed:issn | 1097-4180 | lld:pubmed |
| pubmed-article:18571443 | pubmed:author | pubmed-author:ShevachEthan... | lld:pubmed |
| pubmed-article:18571443 | pubmed:author | pubmed-author:SiegelRichard... | lld:pubmed |
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| pubmed-article:18571443 | pubmed:author | pubmed-author:WangEddie C... | lld:pubmed |
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| pubmed-article:18571443 | pubmed:author | pubmed-author:KahleErinE | lld:pubmed |
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| pubmed-article:18571443 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18571443 | pubmed:day | 18 | lld:pubmed |
| pubmed-article:18571443 | pubmed:volume | 29 | lld:pubmed |
| pubmed-article:18571443 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18571443 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18571443 | pubmed:pagination | 79-89 | lld:pubmed |
| pubmed-article:18571443 | pubmed:dateRevised | 2010-3-15 | lld:pubmed |
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| pubmed-article:18571443 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18571443 | pubmed:articleTitle | The TNF-family receptor DR3 is essential for diverse T cell-mediated inflammatory diseases. | lld:pubmed |
| pubmed-article:18571443 | pubmed:affiliation | Immunoregulation Unit, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892. | lld:pubmed |
| pubmed-article:18571443 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18571443 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18571443 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
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