Revisiting immune exhaustion during HIV infection

被引：168
作者：
Khaitan A. [1 ]
Unutmaz D. [2 ,3 ,4 ]
机构：
[1] Department of Pediatrics, New York University School of Medicine, New York
[2] Department of Microbiology, New York University School of Medicine, New York
[3] Department of Pathology, New York University School of Medicine, New York
[4] Department of Medicine, New York University School of Medicine, New York
来源：
Current HIV/AIDS Reports | 2011年 / 8卷 / 1期
基金：
美国国家卫生研究院;
关键词：
HIV; Immune activation; LAG-3; PD-1; SIV; T-cell exhaustion; Tim-3;
D O I：
10.1007/s11904-010-0066-0
中图分类号：
学科分类号：
摘要：
Chronic immune activation is a hallmark of HIV infection, yet the underlying triggers of immune activation remain unclear. Persistent antigenic stimulation during HIV infection may also lead to immune exhaustion, a phenomenon in which effector T cells become dysfunctional and lose effector functions and proliferative capacity. Several markers of immune exhaustion, such as PD-1, LAG-3, Tim-3, and CTLA-4, which are also negative regulators of immune activation, are preferentially upregulated on T cells during HIV infection. It is not yet clear whether accumulation of T cells expressing activation inhibitory molecules is a consequence of general immune or chronic HIV-specific immune activation. Importantly, however, in vitro blockade of PD-1 and Tim-3 restores HIV-specific T-cell responses, indicating potential for immunotherapies. In this review we discuss the evolution of our understanding of immune exhaustion during HIV infection, highlighting novel markers and potential therapeutic targets. © 2010 Springer Science+Business Media, LLC.
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页码：4 / 11
页数：7
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