| pubmed-article:15004557 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15004557 | lifeskim:mentions | umls-concept:C0023690 | lld:lifeskim |
| pubmed-article:15004557 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:15004557 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:15004557 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:15004557 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:15004557 | lifeskim:mentions | umls-concept:C0021376 | lld:lifeskim |
| pubmed-article:15004557 | lifeskim:mentions | umls-concept:C1539477 | lld:lifeskim |
| pubmed-article:15004557 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:15004557 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:15004557 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:15004557 | pubmed:dateCreated | 2004-3-30 | lld:pubmed |
| pubmed-article:15004557 | pubmed:abstractText | The nonapoptotic functions of Fas ligation are incompletely characterized. In contrast to expectations, we show here that Fas-deficient mice developed less-severe collagen-induced arthritis than did control mice. Despite having milder arthritis, Fas-deficient mice had more of the critical pro-inflammatory mediator interleukin-1 beta (IL-1 beta) in their joints, suggesting inefficient activation through IL-1 receptor 1 (IL-1R1) when Fas signaling is deficient. In primary human macrophages and macrophages from Fas- or Fas ligand (FasL)-deficient mice, interruption of Fas-FasL signaling suppressed nuclear factor-kappa B activation and cytokine expression induced by IL-1 beta and lipopolysaccharide. This cross-talk was mediated by the Fas-associated death domain through interaction with myeloid differentiation factor 88. These observations document a unique mechanism whereby Fas-FasL interactions enhance activation through the IL-1R1 or Toll-like receptor 4 pathway, which may contribute to the pathogenesis of chronic arthritis. | lld:pubmed |
| pubmed-article:15004557 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15004557 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15004557 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15004557 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15004557 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15004557 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15004557 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:15004557 | pubmed:issn | 1529-2908 | lld:pubmed |
| pubmed-article:15004557 | pubmed:author | pubmed-author:PopeRichard... | lld:pubmed |
| pubmed-article:15004557 | pubmed:author | pubmed-author:LiuHongtaoH | lld:pubmed |
| pubmed-article:15004557 | pubmed:author | pubmed-author:IbrahimSaleh... | lld:pubmed |
| pubmed-article:15004557 | pubmed:author | pubmed-author:MaYingyuY | lld:pubmed |
| pubmed-article:15004557 | pubmed:author | pubmed-author:ColeShawn MSM | lld:pubmed |
| pubmed-article:15004557 | pubmed:author | pubmed-author:ThiesenHans-J... | lld:pubmed |
| pubmed-article:15004557 | pubmed:author | pubmed-author:Tu-RappHoangH | lld:pubmed |
| pubmed-article:15004557 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15004557 | pubmed:volume | 5 | lld:pubmed |
| pubmed-article:15004557 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15004557 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15004557 | pubmed:pagination | 380-7 | lld:pubmed |
| pubmed-article:15004557 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15004557 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15004557 | pubmed:articleTitle | Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation. | lld:pubmed |
| pubmed-article:15004557 | pubmed:affiliation | Northwestern University Feinberg School of Medicine and Veteran's Administration Medical Center, Chicago, Lakeside Division, Department of Medicine, Division of Rheumatology, 300 E. Superior Avenue, Tarry 3-713, Chicago, Illinois 60611, USA. | lld:pubmed |
| pubmed-article:15004557 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15004557 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15004557 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:15004557 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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