The regulatory roles of C1q

被引：29
作者：
Lu, Jinhua
Wu, Xiaowei
Teh, Boon King
机构：
[1] Natl Univ Singapore, Dept Microbiol, Yong Loo Lin Sch Med, Singapore 117597, Singapore
[2] Natl Univ Singapore, Program Immunol, Singapore 117597, Singapore
来源：
IMMUNOBIOLOGY | 2007年 / 212卷 / 4-5期
基金：
英国医学研究理事会;
关键词：
C1q; macrophages; dendritic cells; T cells; apoptotic cells; phagocytosis; autoimmunity;
D O I：
10.1016/j.imbio.2006.11.008
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Clq binds to immune complexes to elicit complement-dependent microbial killing and enhance phagocytosis. Besides this classical role, Clq also opsonizes apoptotic cells for clearance by phagocytes. Clq 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 Clq is predominantly synthesized by peripheral tissue macrophages and dendritic cells. Besides being found in the blood, Clq has also been found deposited in extracellular tissues around these cells. In vitro, immobilized Clq 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 Clq in inflammation and autoimmunity. (c) 2006 Elsevier GmbH. All rights reserved.
引用
收藏
页码：245 / 252
页数：8
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