Complement-derived peptide mediators of inflammation.
Complement-derived peptide mediators of inflammation.
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DOI：
10.1093/oxfordjournals.bmb.a072186
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发表时间：
1987-04
影响因子：
6.7
通讯作者：
P. Jose
中科院分区：
文献类型：
--
作者：
P. Jose
血浆和血管外组织液中的补体系统在许多免疫防御反应中起着重要的作用，缺乏功能性的补体系统可以减少许多炎症反应。补体激活通过吞噬、裂解或释放有毒产物来促进急性炎症、白细胞募集和杀死病原体。补体激活的中心事件是C3的裂解，C3a及其代谢物C3a Des Arg的释放。同样，第五个组分的激活导致C5a和C5a des Arg的形成。C3a和C5a是过敏性毒素，因为它们释放组胺并刺激平滑肌收缩。C5衍生的多肽在体外对白细胞有很强的作用，在体内促进中性粒细胞和内皮细胞的相互作用，导致中性粒细胞聚集和相关的水肿形成。
The complement system of blood plasma and extravascular tissue fluid plays an important role in many immune defence reactions and absence of a functional complement system reduces many inflammatory reactions. Complement activation promotes acute inflammation, recruitment of leukocytes and killing of pathogens by phagocytosis, lysis or release of toxic products. The central event in complement activation is cleavage of C3 with the liberation of C3a and its metabolite, C3a des Arg. Similarly, activation of the fifth component results in the formation of C5a and C5a des Arg. C3a and C5a are anaphylatoxins because they release histamine and stimulate smooth muscle contraction. The C5-derived peptides have potent effects on leukocytes in vitro and promote neutrophil-endothelial interactions in vivo which lead to neutrophil accumulation and associated oedema formation.