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细胞凋亡与抗磷脂抗体

Apoptosis and antiphospholipid antibodies.

作者信息

Pittoni V, Isenberg D

机构信息

Centre for Rheumatology, Department of Medicine, University College of London, UK.

出版信息

Semin Arthritis Rheum. 1998 Dec;28(3):163-78. doi: 10.1016/s0049-0172(98)80033-4.

Abstract

OBJECTIVE

To analyze the potential links between antiphospholipid antibodies (aPL) and apoptosis in the pathogenesis of the antiphospholipid antibody syndrome (APS).

METHODS

A review was undertaken of the most relevant scientific literature on apoptosis and autoimmune phenomena. Experimental and human pathology were reviewed to substantiate the hypothesis that apoptosis is involved in the generation of aPL.

RESULTS

Several considerations suggest that exposure of phospholipids (PL) during apoptosis may be a driving antigenic stimulus to the production of aPL. Furthermore, the molecular PL-protein complexes formed during apoptosis are targeted by "pathogenic" aPL. The binding and the clearance of apoptotic cells by these autoantibodies likely further enhances the aPL immune response. Experimental models and human pathology suggest that a restricted genetic background is key to the development of this immune response.

CONCLUSIONS

Abnormalities of apoptosis observed in the course of autoimmune conditions likely provide an antigenic stimulus to the production of aPL.

摘要

目的

分析抗磷脂抗体(aPL)与细胞凋亡在抗磷脂抗体综合征(APS)发病机制中的潜在联系。

方法

对有关细胞凋亡和自身免疫现象的最相关科学文献进行综述。回顾实验和人类病理学以证实细胞凋亡参与aPL产生的假说。

结果

多项因素表明,细胞凋亡期间磷脂(PL)的暴露可能是aPL产生的驱动性抗原刺激。此外,细胞凋亡期间形成的分子PL - 蛋白质复合物是“致病性”aPL的作用靶点。这些自身抗体对凋亡细胞的结合和清除可能进一步增强aPL免疫反应。实验模型和人类病理学表明,有限的遗传背景是这种免疫反应发生发展的关键。

结论

自身免疫性疾病过程中观察到的细胞凋亡异常可能为aPL的产生提供抗原刺激。

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