pubmed-article:15004139 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C0031308 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C0728940 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C0056173 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C1824672 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C0015252 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C1516044 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C1611645 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
pubmed-article:15004139 | lifeskim:mentions | umls-concept:C1627358 | lld:lifeskim |
pubmed-article:15004139 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:15004139 | pubmed:dateCreated | 2004-3-8 | lld:pubmed |
pubmed-article:15004139 | pubmed:abstractText | Human CD93 (known as C1qRp) has been shown to be a phagocytic receptor involved in the in vitro C1q-dependent enhancement of phagocytosis. However, binding of CD93 to C1q and its function remain controversial. In this study, we have generated CD93-deficient mice (CD93(-/-)) to investigate its biological role(s). The CD93(-/-) mice were viable and showed no gross abnormalities in their development. Thioglycolate-elicited peritoneal macrophages deficient in CD93 showed a similar enhancement in complement- and FcgammaR-dependent uptake of RBC to the wild-type macrophages when plated on C1q-coated surfaces suggesting that the lack of this receptor had no effect on these C1q-mediated events. There was no impairment in either complement- or FcgammaR-dependent phagocytic assays in vivo. By contrast, the CD93(-/-) mice had a significant phagocytic defect in the clearance of apoptotic cells in vivo (human Jurkat T cells and murine thymocytes: p=0.0006 and p=0.0079, respectively) compared with strain-matched controls. However, in vitro, the CD93(-/-) macrophages showed similar engulfment of apoptotic cells to wild-type macrophages. Furthermore, no supporting evidence for a role of CD93 as an adhesion molecule was found using intravital microscopy or analyzing peritoneal cell recruitment in response to three different inflammatory stimuli (thioglycolate, zymosan A, and IL-1beta). Thus, our findings indicate that murine CD93 is expressed on the peritoneal macrophage, especially on thioglycolate-elicited cells, but does not appear to play a key role in C1q-mediated enhancement of phagocytosis or in the intercellular adhesion events tested. However, our results suggest that it may contribute to the in vivo clearance of dying cells. | lld:pubmed |
pubmed-article:15004139 | pubmed:language | eng | lld:pubmed |
pubmed-article:15004139 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15004139 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:15004139 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:15004139 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15004139 | pubmed:month | Mar | lld:pubmed |
pubmed-article:15004139 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:15004139 | pubmed:author | pubmed-author:WalportMark... | lld:pubmed |
pubmed-article:15004139 | pubmed:author | pubmed-author:BottoMarinaM | lld:pubmed |
pubmed-article:15004139 | pubmed:author | pubmed-author:Fossati-Jimac... | lld:pubmed |
pubmed-article:15004139 | pubmed:author | pubmed-author:Cortes-Hernan... | lld:pubmed |
pubmed-article:15004139 | pubmed:author | pubmed-author:TaylorPhilip... | lld:pubmed |
pubmed-article:15004139 | pubmed:author | pubmed-author:BygraveAnne... | lld:pubmed |
pubmed-article:15004139 | pubmed:author | pubmed-author:ThompsonRicha... | lld:pubmed |
pubmed-article:15004139 | pubmed:author | pubmed-author:NoursharghSus... | lld:pubmed |
pubmed-article:15004139 | pubmed:author | pubmed-author:NorsworthyPet... | lld:pubmed |
pubmed-article:15004139 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15004139 | pubmed:day | 15 | lld:pubmed |
pubmed-article:15004139 | pubmed:volume | 172 | lld:pubmed |
pubmed-article:15004139 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15004139 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15004139 | pubmed:pagination | 3406-14 | lld:pubmed |
pubmed-article:15004139 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:15004139 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15004139 | pubmed:articleTitle | Murine CD93 (C1qRp) contributes to the removal of apoptotic cells in vivo but is not required for C1q-mediated enhancement of phagocytosis. | lld:pubmed |
pubmed-article:15004139 | pubmed:affiliation | Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus, London, UK. | lld:pubmed |
pubmed-article:15004139 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15004139 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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