Participation of the blood platelet in immune reactions due to platelet-complement interaction.

M O Spycher, U E Nydegger
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引用次数: 14

Abstract

Objective: Review of different aspects of the primary interaction of complement with blood platelets in immunological reactions and the effect on platelet activation in healthy people and patients.

Data sources and selection criteria: Relevant original papers and review articles mainly of the English-written literature.

Results: Besides their major role in hemostasis and wound healing, blood platelets are involved in immunological reactions. They are not only able to interact with IgG through Fc receptors (FcR), they also react with complement components. This review summarizes interactions of complement with mainly human platelets. Such interactions may occur through complement receptors of the plasma membrane (e.g. C1q receptor, complement receptors 2 and 4), but also in a receptor-independent way including activation of the platelet by the membrane attack complex of complement C5b-9. In addition, activation of complement at the surface of the platelets may be induced after binding of anti-platelet antibodies to membrane glycoproteins (e.g. GpIIb/IIIa, GpIb/IX) or after binding of platelet-nonspecific immune complexes via FcR. Complement activation in turn may be regulated by various means including specific plasma or membrane proteins [e.g. decay-accelerating factor (DAF), membrane cofactor protein (MCP), membrane inhibitor of reactive lysis (MIRL), C8-binding protein (C8bp, homologous restriction factor hrf)]. As a further way of self-protection against complement attack, platelets may actively release C5b-9, deposited at the surface as C5b-9-enriched membrane vesicles.

Conclusions: Two lines of interaction of platelet with complement can be distinguished. On the one hand, platelets are equipped with membrane proteins which protect them from complement attack against themselves. On the other hand, membrane receptors for activated complement components as well as for IgG are expressed on the surface, which enable the platelet to intervene in immunological reactions. This property varies between platelets of different species and needs further investigation also in view of the platelet as an intersection between immunology and hemostasis.

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由于血小板-补体相互作用,血小板在免疫反应中的参与。
目的:综述补体与血小板在免疫反应中主要相互作用的不同方面及其对健康人及患者血小板活化的影响。数据来源和选择标准:主要以英文文献为主的相关原创论文和综述文章。结果:血小板除在止血和创面愈合中起主要作用外,还参与免疫反应。它们不仅能通过Fc受体(FcR)与IgG相互作用,还能与补体成分发生反应。本文综述了补体主要与人血小板的相互作用。这种相互作用可能通过质膜上的补体受体(如C1q受体、补体受体2和4)发生,但也可能以不依赖受体的方式发生,包括补体C5b-9的膜攻击复合体激活血小板。此外,抗血小板抗体结合膜糖蛋白(如GpIIb/IIIa, GpIb/IX)或通过FcR结合血小板-非特异性免疫复合物后,可诱导血小板表面补体的活化。补体激活反过来可以通过多种方式调节,包括特定的血浆或膜蛋白[例如,衰变加速因子(DAF),膜辅因子蛋白(MCP),反应性裂解膜抑制剂(MIRL), c8结合蛋白(C8bp,同源限制性内切因子hrf)]。作为对抗补体攻击的另一种自我保护方式,血小板可能主动释放C5b-9,以富含C5b-9的膜泡的形式沉积在表面。结论:血小板与补体的相互作用可区分为两条线。一方面,血小板配备了膜蛋白,保护它们免受补体对自身的攻击。另一方面,活化补体成分的膜受体和IgG的膜受体在表面表达,使血小板能够干预免疫反应。这一特性在不同种类的血小板之间有所不同,鉴于血小板是免疫学和止血之间的交叉点,需要进一步研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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