线粒体琥珀酸促进癌症中的T细胞耗竭。
Mitochondrial succinate feeds T cell exhaustion in cancer.
作者信息
Galluzzi Lorenzo, Guilbaud Emma, Garg Abhishek D
机构信息
Cancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Philadelphia, PA, USA.
Cancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Philadelphia, PA, USA.
出版信息
Cancer Cell. 2025 Feb 10;43(2):168-170. doi: 10.1016/j.ccell.2025.01.005.
PMID:39933894
Abstract
Mitochondrial fitness is critical for effector CD8 T cell responses against cancer. In this issue of Cancer Cell, Ma et al. delineate a novel mechanism linking defects in mitochondrial metabolism as elicited by prolyl 4-hydroxylase subunit alpha 1 (P4HA1) to T cell exhaustion and reduced tumor sensitivity to immunotherapy.
摘要
线粒体健康对于效应性CD8 T细胞对抗癌症的反应至关重要。在本期《癌细胞》杂志中，马等人阐述了一种新机制，该机制将脯氨酰4-羟化酶亚基α1（P4HA1）引发的线粒体代谢缺陷与T细胞耗竭以及肿瘤对免疫疗法的敏感性降低联系起来。
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