Immune Checkpoint Molecules and Glucose Metabolism in HIV-Induced T Cell Exhaustion.
Immune Checkpoint Molecules and Glucose Metabolism in HIV-Induced T Cell Exhaustion.
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DOI：
10.3390/biomedicines10112809
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发表时间：
2022-11-04
期刊：
影响因子：
4.7
通讯作者：
中科院分区：
文献类型：
--
作者：
在人类免疫缺陷病毒（HIV）感染患者中，由于感染触发的细胞耗竭和细胞死亡，CD 8+细胞毒性T细胞的进行性下降与疾病严重程度和进展到危及生命的获得性免疫缺陷综合征（AIDS）阶段显著相关。T细胞耗竭是一种尽管抗原接合但细胞功能障碍的状况，其特征在于免疫检查点分子如程序性细胞死亡蛋白1（PD-1）的表面表达增强，其抑制T细胞受体（TCR）信号传导并对T细胞的增殖和效应子活性产生负面影响。T细胞功能受到细胞葡萄糖代谢的密切调节，细胞葡萄糖代谢产生足够的能量，以支持在对抗病原体感染时的强大反应。在病原体持续存在之后，T细胞从活跃状态到衰竭状态的转变涉及代谢活性的急剧变化。这篇综述强调了免疫检查点分子和葡萄糖代谢之间的相互作用，这有助于在慢性HIV感染的背景下T细胞耗竭，这可以深入了解一种新的治疗策略的合理设计。
The progressive decline of CD8+ cytotoxic T cells in human immunodeficiency virus (HIV)-infected patients due to infection-triggered cell exhaustion and cell death is significantly correlated with disease severity and progression into the life-threatening acquired immunodeficiency syndrome (AIDS) stage. T cell exhaustion is a condition of cell dysfunction despite antigen engagement, characterized by augmented surface expression of immune checkpoint molecules such as programmed cell death protein 1 (PD-1), which suppress T cell receptor (TCR) signaling and negatively impact the proliferative and effector activities of T cells. T cell function is tightly modulated by cellular glucose metabolism, which produces adequate energy to support a robust reaction when battling pathogen infection. The transition of the T cells from an active to an exhausted state following pathogen persistence involves a drastic change in metabolic activity. This review highlights the interplay between immune checkpoint molecules and glucose metabolism that contributes to T cell exhaustion in the context of chronic HIV infection, which could deliver an insight into the rational design of a novel therapeutic strategy.
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DOI：
10.1097/qad.0000000000002007
发表时间：
2018-11-28
期刊：
AIDS (London, England)
影响因子：
--
作者：
Chowdhury FZ;Ouyang Z;Buzon M;Walker BD;Lichterfeld M;Yu XG
通讯作者：
Yu XG
影响因子：
64.5
作者：
Chang CH;Curtis JD;Maggi LB Jr;Faubert B;Villarino AV;O'Sullivan D;Huang SC;van der Windt GJ;Blagih J;Qiu J;Weber JD;Pearce EJ;Jones RG;Pearce EL
通讯作者：
Pearce EL
影响因子：
6.7
作者：
Elahi, Shokrollah;Shahbaz, Shima;Houston, Stan
通讯作者：
Houston, Stan
影响因子：
7.1
作者：
Fernandez-Marcos, Pablo J.;Auwerx, Johan
通讯作者：
Auwerx, Johan
影响因子：
4.4
作者：
Cecchinato, Valentina;Tryniszewska, Elzbieta;Franchini, Genoveffa
通讯作者：
Franchini, Genoveffa