Complement in health and disease

被引:167
|
作者
Carroll, Maria V. [1 ]
Sim, Robert B. [1 ]
机构
[1] Univ Oxford, Dept Pharmacol, Oxford OX1 3QT, England
关键词
Complement; Innate immunity; Blood plasma; Collectins; Inflammation; Phagocytosis; Opsonisation; Autoimmunity; Infection; Disease; MANNOSE-BINDING PROTEIN; PATTERN-RECOGNITION MOLECULES; SYSTEMIC-LUPUS-ERYTHEMATOSUS; HUMAN FACTOR-H; LECTIN PATHWAY ACTIVATION; GUINEA-PIG SERUM; L-FICOLIN; 1ST COMPONENT; ALTERNATIVE-PATHWAY; SERINE PROTEASES;
D O I
10.1016/j.addr.2011.06.005
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The complement system consists of about 35-40 proteins and glycoproteins present in blood plasma or on cell surfaces. Its main biological function is to recognise "foreign" particles and macromolecules, and to promote their elimination either by opsonisation or lysis. Although historically complement has been studied as a system for immune defence against bacteria, it has an important homeostatic role in which it recognises damaged or altered "self" components. Thus complement has major roles in both immune defence against microorganisms, and in clearance of damaged or "used" host components. Since complement proteins opsonise or lyse cells, complement can damage healthy host cells and tissues. The system is regulated by many endogenous regulatory proteins. Regulation is sometimes imperfect and both too much and too little complement activation is associated with many diseases. Excessive or inappropriate activation can cause tissue damage in diseases such as rheumatoid arthritis, age-related macular degeneration (AMD), multiple sclerosis, ischemia-reperfusion injury (e.g. ischemic stroke). Insufficient complement activity is associated with susceptibility to infection (mainly bacterial) and development of autoimmune disease, like SLE (systemic lupus erythematosus). (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:965 / 975
页数:11
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