| pubmed-article:15670831 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15670831 | lifeskim:mentions | umls-concept:C0524914 | lld:lifeskim |
| pubmed-article:15670831 | lifeskim:mentions | umls-concept:C1411976 | lld:lifeskim |
| pubmed-article:15670831 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:15670831 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
| pubmed-article:15670831 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:15670831 | pubmed:dateCreated | 2005-1-26 | lld:pubmed |
| pubmed-article:15670831 | pubmed:abstractText | The response of Toll-like receptor 4 (TLR4) to lipopolysaccharide (LPS) is thought vital for resisting infection. Since aberrant TLR4 signaling may initiate inflammatory conditions such as the sepsis syndrome, we sought a component of normal cells that might provide local control of TLR4 activation. We found that antibodies that block chemokine receptor 4 (CXCR4) function enhanced TLR4 signaling, while increased expression of CXCR4 or addition of the CXCR4 ligand SDF-1 suppressed TLR4 signaling induced by LPS. These findings suggest that CXCR4 could exert local control of TLR4 and suggest the possibility of new therapeutic approaches to suppression of TLR4 function. | lld:pubmed |
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| pubmed-article:15670831 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15670831 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15670831 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15670831 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15670831 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15670831 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:15670831 | pubmed:issn | 0014-5793 | lld:pubmed |
| pubmed-article:15670831 | pubmed:author | pubmed-author:PlattJeffrey... | lld:pubmed |
| pubmed-article:15670831 | pubmed:author | pubmed-author:BrunnGregory... | lld:pubmed |
| pubmed-article:15670831 | pubmed:author | pubmed-author:KishoreSandee... | lld:pubmed |
| pubmed-article:15670831 | pubmed:author | pubmed-author:BungumMarlo... | lld:pubmed |
| pubmed-article:15670831 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15670831 | pubmed:day | 31 | lld:pubmed |
| pubmed-article:15670831 | pubmed:volume | 579 | lld:pubmed |
| pubmed-article:15670831 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15670831 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15670831 | pubmed:pagination | 699-704 | lld:pubmed |
| pubmed-article:15670831 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:15670831 | pubmed:meshHeading | pubmed-meshheading:15670831... | lld:pubmed |
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| pubmed-article:15670831 | pubmed:meshHeading | pubmed-meshheading:15670831... | lld:pubmed |
| pubmed-article:15670831 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15670831 | pubmed:articleTitle | Selective suppression of Toll-like receptor 4 activation by chemokine receptor 4. | lld:pubmed |
| pubmed-article:15670831 | pubmed:affiliation | Transplantation Biology, Mayo Clinic, 200 First Street SW, Medical Sciences 2-66, Rochester, MN 55905, USA. | lld:pubmed |
| pubmed-article:15670831 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15670831 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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