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Apoptosis and antiphospholipid antibodies.

机译:凋亡和抗磷脂抗体。

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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.
机译:目的:分析抗磷脂抗体综合征(APS)发病机理中抗磷脂抗体(aPL)与细胞凋亡之间的潜在联系。方法:回顾了有关细胞凋亡和自身免疫现象的最相关的科学文献。审查了实验和人类病理学,以证实细胞凋亡与aPL产生有关的假说。结果:一些考虑因素表明,细胞凋亡过程中磷脂(PL)的暴露可能是aPL产生的驱动性抗原刺激。此外,在细胞凋亡期间形成的分子PL-蛋白质复合物被“致病性” aPL靶向。这些自身抗体对凋亡细胞的结合和清除可能会进一步增强aPL免疫反应。实验模型和人体病理学表明,有限的遗传背景是这种免疫反应发展的关键。结论:在自身免疫性疾病过程中观察到的凋亡异常可能为aPL的产生提供了抗原刺激。

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