Apoptosis of uninfected cells induced by HIV envelope glycoproteins.
Apoptosis of uninfected cells induced by HIV envelope glycoproteins.
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DOI：
10.1186/1742-4690-1-12
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发表时间：
2004-06-23
期刊：
影响因子：
3.3
通讯作者：
Biard-Piechaczyk M
中科院分区：
文献类型：
--
作者：
Ahr B;Robert-Hebmann V;Devaux C;Biard-Piechaczyk M
细胞凋亡，或程序性细胞死亡，是生物稳态的关键事件，但也参与了许多人类疾病的发病机制，包括人类免疫缺陷病毒(HIV)感染。虽然HIV感染者的T细胞逐渐减少有多种机制，但未感染的旁观者T细胞，包括CD4+和CD8+T细胞的程序性死亡是导致免疫缺陷的重要事件。HIV包膜糖蛋白(Env)在与其受体、CD4分子和辅受体(主要是CCR5和CXCR4)结合后，在传递这种凋亡信号方面发挥了关键作用。根据Env的呈现、参与的受体和靶细胞接触的复杂性，细胞凋亡诱导与死亡受体和/或线粒体依赖的途径有关。本文综述了目前关于Env介导的细胞死亡导致T细胞耗竭和临床并发症的知识，并涵盖了解决T细胞死亡的可能机制的一些有时相互矛盾的研究。
Apoptosis, or programmed cell death, is a key event in biologic homeostasis but is also involved in the pathogenesis of many human diseases including human immunodeficiency virus (HIV) infection. Although multiple mechanisms contribute to the gradual T cell decline that occurs in HIV-infected patients, programmed cell death of uninfected bystander T lymphocytes, including CD4+ and CD8+ T cells, is an important event leading to immunodeficiency. The HIV envelope glycoproteins (Env) play a crucial role in transducing this apoptotic signal after binding to its receptors, the CD4 molecule and a coreceptor, essentially CCR5 and CXCR4. Depending on Env presentation, the receptor involved and the complexity of target cell contact, apoptosis induction is related to death receptor and/or mitochondria-dependent pathways. This review summarizes current knowledge of Env-mediated cell death leading to T cell depletion and clinical complications and covers the sometimes conflicting studies that address the possible mechanisms of T cell death.