时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
Activated effector T cells increase aerobic glycolysis to support rapid proliferation and cytokine production; however, mitochondrial metabolism remains essential for signalling competence, biosynthetic reactions and the establishment of long‐lived or regulatory states [].
方法
The process under consideration may enable delivery of functional mitochondria to a cohort of T cells that are metabolically compromised.；All authors read and approved the final version of the manuscript.
核心结论
Activated effector T cells increase aerobic glycolysis to support rapid proliferation and cytokine production; however, mitochondrial metabolism remains essential for signalling competence, biosynthetic reactions and the establishment of long‐lived or regulatory states [].；In instances where these adaptive mechanisms are compromised, mitochondria can become a significant contributor to the onset of T‐cell dysfunction.；These proteins act as stress sensors, modulating the activation of BAX/BAK‐mediated mitochondrial outer‐membrane permeabilisation in response to declining cytokine‐ or antigen‐derived survival signals [, ]. ‖ 结论：In conclusion, the studies discussed throughout this review support the view that mitochondria are not merely bioenergetic “support units” in T cells, but rather dynamic hubs that integrate metabolism with signalling, differentiation, and long‐term immune fitness [].
局限
In future studies, it will be crucial to establish the context‐dependency of these strategies, identify robust biomarkers of mitochondrial competence in T‐cell subsets (including Tpex populations), and elucidate the causal relationships between mitochondrial remodelling and immune outcomes.；Overall, the central message emerging from this review is that mitochondrial dysfunction should be interpreted as an active determinant of T‐cell fate rather than as a secondary metabolic consequence of chronic immune stimulation.
对本项目的价值
★☆☆☆☆ 炎症衰老是几乎所有慢性老年病的公共通路，也是最有希望做「抗炎但保留免疫」解耦的靶点。
全文来源
PMC JATS 全文（正文 56,404 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Broken Engines of Immunity: Mitochondrial Dysfunction in T Cells Across Cancer and Complex Pathologies.
- 期刊与标识：Eur J Immunol · PMID 42947567 · DOI 10.1002/eji.70300
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