Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.imbio.2006.11.008
Title: The regulatory roles of C1q
Authors: Lu, J. 
Wu, X.
Teh, B.K.
Keywords: Apoptotic cells
Autoimmunity
C1q
Dendritic cells
Macrophages
Phagocytosis
T cells
Issue Date: 2007
Source: Lu, J., Wu, X., Teh, B.K. (2007). The regulatory roles of C1q. Immunobiology 212 (4-5) : 245-252. ScholarBank@NUS Repository. https://doi.org/10.1016/j.imbio.2006.11.008
Abstract: C1q binds to immune complexes to elicit complement-dependent microbial killing and enhance phagocytosis. Besides this classical role, C1q also opsonizes apoptotic cells for clearance by phagocytes. C1q deficiency increases susceptibility to microbial infections and is also associated with elevated autoimmunity as characterized by increased apoptotic bodies in tissues. Most complement proteins are of liver origin, but C1q is predominantly synthesized by peripheral tissue macrophages and dendritic cells. Besides being found in the blood, C1q has also been found deposited in extracellular tissues around these cells. In vitro, immobilized C1q inhibits monocyte, macrophage and T-cell production of inflammatory cytokines. It also regulates T-cell activation. Therefore, mounting evidence suggest a major regulatory role for C1q in inflammation and autoimmunity. © 2006 Elsevier GmbH. All rights reserved.
Source Title: Immunobiology
URI: http://scholarbank.nus.edu.sg/handle/10635/24663
ISSN: 01712985
DOI: 10.1016/j.imbio.2006.11.008
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