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T细胞耗竭中的线粒体代谢

Mitochondrial Metabolism in T-Cell Exhaustion.

作者信息

Li Fei, Feng Yu, Yin Zesheng, Wang Yahong

机构信息

Institute of Pathogen Biology, School of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, China.

School of Public Health, Lanzhou University, Lanzhou 730000, China.

出版信息

Int J Mol Sci. 2025 Jul 31;26(15):7400. doi: 10.3390/ijms26157400.

Abstract

T cells play a vital role in resisting pathogen invasion and maintaining immune homeostasis. However, T cells gradually become exhausted under chronic antigenic stimulation, and this exhaustion is closely related to mitochondrial dysfunction in T cells. Mitochondria play a crucial role in the metabolic reprogramming of T cells to achieve the desired immune response. Here, we compiled the latest research on how mitochondrial metabolism determines T cell function and differentiation, with the mechanisms mainly including mitochondrial biogenesis, fission, fusion, mitophagy, and mitochondrial transfer. In addition, the alterations in mitochondrial metabolism in T-cell exhaustion were also reviewed. Furthermore, we discussed intervention strategies targeting mitochondrial metabolism to reverse T cell exhaustion in detail, including inducing PGC-1α expression, alleviating reactive oxygen species (ROS) production or hypoxia, enhancing ATP production, and utilizing mitochondrial transfer. Targeting mitochondrial metabolism in exhausted T cells may achieve the goal of reversing and preventing T cell exhaustion.

摘要

T细胞在抵抗病原体入侵和维持免疫稳态中发挥着至关重要的作用。然而,在慢性抗原刺激下,T细胞会逐渐耗竭,而这种耗竭与T细胞中的线粒体功能障碍密切相关。线粒体在T细胞的代谢重编程中发挥着关键作用,以实现所需的免疫反应。在此,我们汇总了关于线粒体代谢如何决定T细胞功能和分化的最新研究,其机制主要包括线粒体生物发生、裂变、融合、线粒体自噬和线粒体转移。此外,还综述了T细胞耗竭中线粒体代谢的改变。此外,我们详细讨论了针对线粒体代谢以逆转T细胞耗竭的干预策略,包括诱导PGC-1α表达、减轻活性氧(ROS)产生或缺氧、增强ATP产生以及利用线粒体转移。针对耗竭T细胞中的线粒体代谢可能实现逆转和预防T细胞耗竭的目标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a42/12347488/b9453caaacb4/ijms-26-07400-g001.jpg

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