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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
immunology and microbiology
Human complement Factor H modulates C1q-mediated phagocytosis of apoptotic cells
Immunobiology, Volume 217, No. 4, Year 2012
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Description
Complement is implicated in the clearance of apoptotic cells by phagocytes. Deficiencies in early complement components, particularly C1q, are associated with an increased risk of the development of systemic lupus erythematosus. C1q is considered to be important in this process through interaction with apoptotic cells and phagocytes. In the present study, we confirm that apoptotic cells are recognized not only by C1q but also by the complement regulatory protein Factor H. Both C1q and Factor H bind to apoptotic cells in a dose-dependent and saturable manner. We further examined the role of C1q and Factor H in the clearance of apoptotic cells by monocytes. C1q enhanced uptake/adhesion of apoptotic cells by monocytes whereas Factor H alone had no effect on this process. However, when both C1q and Factor H were present on the apoptotic cell surface, C1q-mediated enhancement of uptake/adhesion of the apoptotic cells by monocytes was reduced. This effect of Factor H also occurred if monocytes were pre-treated with Factor H, and then exposed to C1q-coated apoptotic cells. The results were consistent with Factor H interacting with monocytes through the integrin CD11b/CD18. We conclude that under physiological conditions, Factor H may be important in controlling the inflammation which might arise from C1q deposition on apoptotic cells. © 2011 Elsevier GmbH.
Authors & Co-Authors
Kang, Yuhoi
United Kingdom, Oxford
University of Oxford Medical Sciences Division
United Kingdom, Oxford
Nuffield Department of Medicine
Urban, Britta Christina
United Kingdom, Oxford
University of Oxford
Kenya, Nairobi
Wellcome Trust Research Laboratories Nairobi
Sim, Robert B.
United Kingdom, Oxford
University of Oxford Medical Sciences Division
United Kingdom, Oxford
University of Oxford
Kishore, Uday
United Kingdom, Uxbridge
Brunel University London
Statistics
Citations: 41
Authors: 4
Affiliations: 5
Identifiers
Doi:
10.1016/j.imbio.2011.10.008
ISSN:
01712985
e-ISSN:
18783279