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HIV感染中CD4+ T细胞耗竭:死于“友军火力”?

CD4+ T-cell depletion in HIV infection: killed by friendly fire?

作者信息

Moanna Abeer, Dunham Richard, Paiardini Mirko, Silvestri Guido

机构信息

Emory Vaccine Center, Emory University School of Medicine, 954 Gatewood Road NE, Atlanta, GA 30329, USA.

出版信息

Curr HIV/AIDS Rep. 2005 Feb;2(1):16-23. doi: 10.1007/s11904-996-0004-3.

DOI:10.1007/s11904-996-0004-3
PMID:16091244
Abstract

Recent studies have emphasized the role of a chronic, generalized activation of the immune system as a prominent cause of CD4+ T-cell depletion in HIV-infected patients. The HIV-induced immune activation is a strong predictor of disease progression in humans, and lack of immune activation is a key feature of nonpathogenic simian immunodeficiency virus (SIV) infection of natural hosts. The mechanisms by which immune activation induces CD4+ T-cell depletion are still incompletely understood, but likely involve changes in the complex dynamics of the naive, memory, and effector subsets of T cells. A better understanding of how HIV-induced immune activation leads to CD4+ T-cell depletion may provide new targets for immune-based interventions that could be used, in addition to standard antiretroviral therapy, to slow disease progression in HIV-infected individuals.

摘要

最近的研究强调,免疫系统的慢性全身性激活是导致HIV感染患者CD4+ T细胞耗竭的一个主要原因。HIV诱导的免疫激活是人类疾病进展的一个强有力预测指标,而缺乏免疫激活是非致病性猿猴免疫缺陷病毒(SIV)感染天然宿主的一个关键特征。免疫激活诱导CD4+ T细胞耗竭的机制仍未完全明了,但可能涉及T细胞的初始、记忆和效应亚群复杂动态变化。更好地理解HIV诱导的免疫激活如何导致CD4+ T细胞耗竭,可能为基于免疫的干预措施提供新靶点,除标准抗逆转录病毒疗法外,这些靶点可用于减缓HIV感染个体的疾病进展。

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