Navratil Jeannine S, Liu Chau-Ching, Ahearn Joseph M
Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
Immunol Res. 2006;36(1-3):3-12. doi: 10.1385/IR:36:1:3.
Cell death by apoptosis plays a significant and seemingly contradictory role in the development and pathogenesis of autoimmune diseases. Apoptosis is integral to the assembly and maintenance of a healthy, self-tolerant immune system. However, many of the molecular and cellular events specific to apoptosis generate a reservoir of self-antigens with the potential to initiate and possibly perpetuate autoimmune conditions. Recent findings that support this latter, more sinister role for apoptosis have shed light on a mystery that is common to many systemic autoimmune diseases, namely, why the majority of autoantibodies produced in patients with these diseases target proteins that are normally found inside the cell, often within the nucleus. This review will discuss how autoantigens are specifically altered during the apoptotic process, and how the complement system participates in recognizing and clearing these potentially immunogenic packages.
凋亡引起的细胞死亡在自身免疫性疾病的发展和发病机制中发挥着重要且看似矛盾的作用。凋亡对于健康的、具有自身耐受性的免疫系统的组装和维持不可或缺。然而,许多凋亡特有的分子和细胞事件会产生自身抗原库,这些自身抗原有可能引发并可能使自身免疫状态持续存在。最近的研究结果支持了凋亡的这一更为有害的作用,揭示了许多系统性自身免疫性疾病共有的一个谜团,即为什么这些疾病患者产生的大多数自身抗体靶向通常存在于细胞内、 often within the nucleus. 本文将讨论自身抗原在凋亡过程中是如何被特异性改变的,以及补体系统如何参与识别和清除这些潜在的免疫原性包裹。 (注:原文中“often within the nucleus”后面似乎缺少内容,但按照要求完整翻译了现有文本)