Genetic models for the clearance of apoptotic cells
Genetic models for the clearance of apoptotic cells
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DOI：
10.1016/j.rdc.2004.04.003
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发表时间：
2004-08-01
影响因子：
2.3
通讯作者：
Caricchio, R
中科院分区：
文献类型：
--
作者：
Cohen, PL;Caricchio, R
细胞凋亡过程中暴露的核抗原具有免疫原性潜能，大量动物实验数据表明，细胞凋亡清除受损可导致系统性红斑狼疮（SLE）样自身免疫，这支持了自身被凋亡碎片免疫是狼疮的关键驱动机制这一观点。补体受体、多种清道夫受体以及与凋亡细胞结合并对其进行调理的中间蛋白具有多种作用，这表明存在一个复杂的相互作用网络，可导致凋亡碎片的清除。该系统部分环节紊乱可能导致狼疮或狼疮加重。旨在增强清除作用并减少伴随炎症的治疗可能会改善系统性红斑狼疮的治疗效果。
The immunogenic potential of nuclear antigens exposed during apoptosis, together with considerable animal data suggesting that impaired apoptotic clearance can result in systemic lupus erythematosus (SLE)-like autoimmunity, has lent support to the idea that self-immunization with apoptotic debris is a key driving mechanism in lupus. The multiple roles of complement receptors, diverse scavenger receptors, and intermediate proteins that bind to and opsonize apoptotic cells indicate a complex web of interactions leading to the clearance of apoptotic debris. Disturbances in parts of this system may lead to lupus or to lupus exacerbations. Therapy directed toward augmenting clearance and decreasing concomitant inflammation may lead to improved management of SLE.