{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T12:16:13Z","timestamp":1791288973619,"version":"4.3.0"},"reference-count":32,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2004,3,1]],"date-time":"2004-03-01T00:00:00Z","timestamp":1078099200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>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\u2212\/\u2212) to investigate its biological role(s). The CD93\u2212\/\u2212 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 Fc\u03b3R-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 Fc\u03b3R-dependent phagocytic assays in vivo. By contrast, the CD93\u2212\/\u2212 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\u2212\/\u2212 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-1\u03b2). 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.<\/jats:p>","DOI":"10.4049\/jimmunol.172.6.3406","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T21:59:29Z","timestamp":1398031169000},"page":"3406-3414","source":"Crossref","is-referenced-by-count":125,"title":["Murine CD93 (C1qRp) Contributes to the Removal of Apoptotic Cells In Vivo but Is Not Required for C1q-Mediated Enhancement of Phagocytosis"],"prefix":"10.1093","volume":"172","author":[{"given":"Peter J","family":"Norsworthy","sequence":"first","affiliation":[{"name":"Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liliane","family":"Fossati-Jimack","sequence":"additional","affiliation":[{"name":"Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Josefina","family":"Cortes-Hernandez","sequence":"additional","affiliation":[{"name":"Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip R","family":"Taylor","sequence":"additional","affiliation":[{"name":"Sir William Dunn School of Pathology, University of Oxford , Oxford ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne E","family":"Bygrave","sequence":"additional","affiliation":[{"name":"Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard D","family":"Thompson","sequence":"additional","affiliation":[{"name":"Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sussan","family":"Nourshargh","sequence":"additional","affiliation":[{"name":"Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark J","family":"Walport","sequence":"additional","affiliation":[{"name":"Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marina","family":"Botto","sequence":"additional","affiliation":[{"name":"Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2004,3,15]]},"reference":[{"key":"2026020211191321700_R1","first-page":"250","volume-title":"Immunobiology","year":"1998"},{"key":"2026020211191321700_R2","first-page":"407","volume-title":"Immunobiology","year":"2002"},{"key":"2026020211191321700_R3","first-page":"3583","volume-title":"J. 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