The regulatory roles of C1q.
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.
Lu
Jinhua
J
Department of Microbiology, Yong Loo Lin School of Medicine and NUS Immunology Program, National University of Singapore, Blk MD4, 5 Science Drive 2, Singapore 117597, Singapore. miclujh@nus.edu.sg
Wu
Xiaowei
X
Teh
Boon King
BK
D000818:Animals; D017209:Apoptosis; D015551:Autoimmunity / Q000276:immunology; D015922:Complement C1q / Q000276:immunology* / Q000378:metabolism*; D003176:Complement C3 / Q000276:immunology / Q000378:metabolism; D003171:Complement Pathway, Classical / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis; D003713:Dendritic Cells / Q000378:metabolism; D006801:Humans; D008264:Macrophages / Q000378:metabolism; D010587:Phagocytosis; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism
D003176:Complement C3; D016207:Cytokines; D015922:Complement C1q