Platelets as effectors in immune and hypersensitivity reactions.
Platelets as effectors in immune and hypersensitivity reactions.
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血小板作为免疫和超敏反应的效应器。
DOI：
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发表时间：
1987
期刊：
影响因子：
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通讯作者：
C. Auriault
中科院分区：
文献类型：
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作者：
A. Capron;M. Joseph;J. Ameisen;M. Capron;V. Pancré;C. Auriault
最近在人血小板上发现了IgE受体。这些受体在之前描述的巨噬细胞和嗜酸性粒细胞的Fc epsilon R2中具有共同的特性，Ka为3 X 10(7) M-1，每个血小板的IgE结合位点平均为600-1,000。抗fc epsilon R2单克隆抗体的生产已经允许在43-45和31 kD两个主要条带的血小板膜制剂上进行鉴定。在寄生虫感染（血吸虫病、丝虫病）中，已证实血小板对ige依赖性杀伤。在过敏性哮喘和膜翅目毒液敏感患者中，通过释放细胞杀伤介质和氧化破裂表达的ige依赖性血小板活化可被相应的过敏原特异性触发。在阿司匹林敏感哮喘中，已证实非甾体抗炎药可直接激活非ige依赖性血小板。血小板异常显然与前列腺素H2与其特异性受体结合的缺陷以及脂氧合酶代谢物调节功能的可能失衡有关。血小板效应功能最近被证明是由T细胞因子调节的。OKT8 T细胞亚群产生的一种新的抑制性淋巴因子（PASL）抑制血小板激活和杀伤，而ifn - γ已经在OKT4+细胞产生的能够触发血小板激活的T细胞因子中被鉴定出来。这些观察结果为过敏性和假性过敏性疾病的发病机制、诊断和预防开辟了新的视角，并为血小板在各种免疫和超敏反应中的作用提供了支持。
IgE receptors have been recently characterized on human blood platelets. These receptors share common properties within the Fc epsilon R2 previously described on macrophages and eosinophils with a Ka of 3 X 10(7) M-1 and a mean number of 600-1,000 binding sites for IgE per platelet. The production of an anti-Fc epsilon R2 monoclonal antibody has allowed the identification on platelet membrane preparations of two major bands of 43-45 and 31 kD. In parasitic infections (schistosomiasis, filariasis) IgE-dependent killing by platelets has been demonstrated. In allergic asthma and in Hymenoptera venom sensitivity patients, IgE-dependent activation of platelets expressed by the release of cytocidal mediators and oxidative burst can be specifically triggered by the corresponding allergen. In aspirin-sensitive asthma, a direct, non-IgE-dependent platelet activation by nonsteroidal anti-inflammatory drugs has been demonstrated. The platelet abnormality apparently involved a defect of the prostaglandin H2 binding to its specific receptor and a possible imbalance in the regulatory functions of the lipoxygenase metabolites. Platelet effector functions have been recently shown to be regulated by T cell factors. A novel suppressive lymphokine (PASL) produced by OKT8 T cell subset inhibits platelet activation and killing whereas IFN-gamma has been identified among T cell factors produced by OKT4+ cells able to trigger platelet activation. These observations open original perspectives into the pathogenesis, the diagnosis and the prevention of allergic and pseudoallergic disorders, and they provide support to the concept of a role for platelets in various immune and hypersensitivity reactions.