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末端补体序列的功能及相关性

Functions and relevance of the terminal complement sequence.

作者信息

Bhakdi S, Hugo F, Tranum-Jensen J

机构信息

Institute of Medical Microbiology, University of Giessen, Federal Republic of Germany.

出版信息

Blut. 1990 Jun;60(6):309-18. doi: 10.1007/BF01737843.

DOI:10.1007/BF01737843
PMID:2198074
Abstract

The terminal complement sequence is initiated upon cleavage of C5 with liberation of C5a anaphylatoxin, and involves the assembly of macromolecular C5b-9 complexes either on cell surfaces or in plasma. Cell-bound C5b-9 complexes generate transmembrane pores that can cause cell death, or they can elicit secondary cellular reactions triggered, for example, by passive flux of calcium ions into the cells. In vivo functions of the fluid-phase SC5b-9 complex have not yet been defined, but the identity of S-protein with vitronectin (serum spreading factor) provokes the anticipation that significant biological functions of this complex do exist. The terminal complement sequence may fulfil protective functions when it is triggered on alien cells that are marked for destruction. Dysregulation in the complement sequence may, however, result in detrimental attack by C5b-9 on autologous cells. Examples include not only autoimmune disease states, but also the activation of complement on dead or dying cells, and bystander attack on blood cells during cardiopulmonary bypass. Methods for detecting and quantifying C5b-9 are outlined, and the potential usefulness of such assays in clinical research is discussed.

摘要

补体终末序列在C5裂解并释放过敏毒素C5a时启动,涉及在细胞表面或血浆中组装大分子C5b-9复合物。细胞结合的C5b-9复合物会产生跨膜孔,可导致细胞死亡,或者引发继发性细胞反应,例如由钙离子被动流入细胞所触发的反应。液相SC5b-9复合物的体内功能尚未明确,但S蛋白与玻连蛋白(血清扩散因子)的一致性引发了人们对该复合物确实存在重要生物学功能的预期。当补体终末序列在外来细胞上触发时,可能发挥保护作用,这些外来细胞被标记以待破坏。然而,补体序列的失调可能导致C5b-9对自体细胞的有害攻击。例子不仅包括自身免疫疾病状态,还包括补体在死亡或濒死细胞上的激活,以及体外循环期间对血细胞的旁观者攻击。概述了检测和定量C5b-9的方法,并讨论了此类检测在临床研究中的潜在用途。

相似文献

1
Functions and relevance of the terminal complement sequence.末端补体序列的功能及相关性
Blut. 1990 Jun;60(6):309-18. doi: 10.1007/BF01737843.
2
[Functions and relevance of the terminal complement sequence].
Immun Infekt. 1990 Jun;18(3):71-9.
3
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Inhibiting the C5-C5a receptor axis.抑制 C5-C5a 受体轴。
Mol Immunol. 2011 Aug;48(14):1631-42. doi: 10.1016/j.molimm.2011.04.014. Epub 2011 May 6.
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Relative inefficiency of terminal complement activation.末端补体激活的相对低效性。
J Immunol. 1988 Nov 1;141(9):3117-22.
6
Studies on the mechanism of bacterial resistance to complement-mediated killing. VI. IgG increases the bactericidal efficiency of C5b-9 for E. coli 0111B4 by acting at a step before C5 cleavage.细菌对补体介导杀伤作用的抗性机制研究。VI. IgG通过在C5裂解前的一个步骤发挥作用,提高C5b-9对大肠杆菌0111B4的杀菌效率。
J Immunol. 1983 Nov;131(5):2570-5.
7
The pathobiology of the terminal complement complexes.终末补体复合物的病理生物学
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8
Pathways of complement activation in membranoproliferative glomerulonephritis and allograft rejection.膜增生性肾小球肾炎和同种异体移植排斥反应中补体激活途径。
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9
Deposition of terminal C5b-9 complement complexes on erythrocytes and leukocytes during cardiopulmonary bypass.体外循环期间终末C5b-9补体复合物在红细胞和白细胞上的沉积。
N Engl J Med. 1988 Feb 18;318(7):408-14. doi: 10.1056/NEJM198802183180704.
10
Noncytolytic terminal complement complexes may serve as calcium gates to elicit leukotriene B4 generation in human polymorphonuclear leukocytes.非溶细胞性末端补体复合物可能作为钙通道,引发人多形核白细胞中白三烯B4的生成。
J Immunol. 1986 Aug 15;137(4):1286-93.

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Malarial anemia: digestive vacuole of Plasmodium falciparum mediates complement deposition on bystander cells to provoke hemophagocytosis.疟原虫贫血:恶性疟原虫的消化空泡介导补体在旁观者细胞上沉积,引发噬血现象。
Med Microbiol Immunol. 2014 Dec;203(6):383-93. doi: 10.1007/s00430-014-0347-0. Epub 2014 Jul 2.
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Complement activation and formation of the membrane attack complex on serogroup B Neisseria meningitidis in the presence or absence of serum bactericidal activity.在有或无血清杀菌活性的情况下,B群脑膜炎奈瑟菌补体激活及膜攻击复合物的形成。
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3

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Homologous species restriction in lysis of erythrocytes by terminal complement proteins.终末补体蛋白对红细胞溶解的同源物种限制
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Macrophages release arachidonic acid, prostaglandin E2, and thromboxane in response to late complement components.巨噬细胞会响应补体晚期成分而释放花生四烯酸、前列腺素E2和血栓素。
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