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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0015252,
umls-concept:C0031308,
umls-concept:C0056173,
umls-concept:C0591833,
umls-concept:C0728940,
umls-concept:C1515655,
umls-concept:C1516044,
umls-concept:C1611645,
umls-concept:C1627358,
umls-concept:C1824672,
umls-concept:C1880177,
umls-concept:C2349975
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pubmed:issue |
6
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pubmed:dateCreated |
2004-3-8
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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.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adjuvants, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD44,
http://linkedlifedata.com/resource/pubmed/chemical/C1QBP protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/C1qbp protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C1q,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Opsonin Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgG,
http://linkedlifedata.com/resource/pubmed/chemical/Thioglycolates,
http://linkedlifedata.com/resource/pubmed/chemical/complement 1q receptor
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
172
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3406-14
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15004139-Adjuvants, Immunologic,
pubmed-meshheading:15004139-Animals,
pubmed-meshheading:15004139-Antigens, CD44,
pubmed-meshheading:15004139-Apoptosis,
pubmed-meshheading:15004139-Carrier Proteins,
pubmed-meshheading:15004139-Cell Movement,
pubmed-meshheading:15004139-Cells, Cultured,
pubmed-meshheading:15004139-Complement C1q,
pubmed-meshheading:15004139-Complement C3,
pubmed-meshheading:15004139-Erythrocytes,
pubmed-meshheading:15004139-Gene Targeting,
pubmed-meshheading:15004139-Humans,
pubmed-meshheading:15004139-Immunoglobulin G,
pubmed-meshheading:15004139-Jurkat Cells,
pubmed-meshheading:15004139-Macrophage Activation,
pubmed-meshheading:15004139-Macrophages, Peritoneal,
pubmed-meshheading:15004139-Membrane Glycoproteins,
pubmed-meshheading:15004139-Mice,
pubmed-meshheading:15004139-Mice, Inbred C57BL,
pubmed-meshheading:15004139-Mice, Knockout,
pubmed-meshheading:15004139-Mitochondrial Proteins,
pubmed-meshheading:15004139-Opsonin Proteins,
pubmed-meshheading:15004139-Phagocytosis,
pubmed-meshheading:15004139-Receptors, Complement,
pubmed-meshheading:15004139-Receptors, IgG,
pubmed-meshheading:15004139-Sequence Deletion,
pubmed-meshheading:15004139-T-Lymphocyte Subsets,
pubmed-meshheading:15004139-Thioglycolates
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pubmed:year |
2004
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pubmed:articleTitle |
Murine CD93 (C1qRp) contributes to the removal of apoptotic cells in vivo but is not required for C1q-mediated enhancement of phagocytosis.
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pubmed:affiliation |
Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus, London, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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