Apoptosis in the pathogenesis of systemic lupus erythematosus
Apoptosis in the pathogenesis of systemic lupus erythematosus
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DOI：
10.1177/0961203308089990
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发表时间：
2008-01-01
期刊：
影响因子：
2.6
通讯作者：
van der Vlag, J.
中科院分区：
文献类型：
--
作者：
Munoz, L. E.;van Bavel, C.;van der Vlag, J.
系统性红斑狼疮（SLE）是一种典型的炎症性自身免疫性疾病，由自身免疫应答核自身抗原引起。在细胞凋亡过程中，许多狼疮自身抗原聚集在细胞内，易受修饰。修改过的核成分被认为是外来的和危险的。因此，凋亡细胞必须被有效清除，以避免凋亡碎片的积累和随后的自身免疫反应的发展。因此，凋亡和凋亡细胞/物质的清除被认为是SLE病因学的关键过程。清除缺陷可能通过诱导淋巴组织的耐受性丧失来解释自身免疫的发展。此外，在自身抗体存在的情况下，凋亡细胞的吞噬可能导致促炎反应。这可能会维持炎症状况和显性狼疮的病理。
Systemic lupus erythematosus (SLE) is a prototype inflammatory autoimmune disease resulting from autoimmune responses against nuclear autoantigens. During apoptosis many lupus autoantigens congregate inside the cells and are susceptible to modifications. Modified nuclear constituents are considered foreign and dangerous. Therefore, apoptotic cells have to has to be efficiently removed to avoid the accumulation of apoptotic debris and the subsequently development of autoimmune responses. Hence, apoptosis and clearance of apoptotic cells/material are considered key processes in the aetiology of SLE. Clearance deficiencies may account for the development of auto-immunity by inducing a loss of tolerance in lymphoid tissues. Furthermore, phagocytosis of apoptotic cells may lead to a pro-inflammatory response in the presence of autoantibodies. This may sustain inflammatory conditions and the pathology found in overt lupus.