Qiu Yajing, Xu Yihan, Ding Xinyuan, Zhao Congcong, Cheng Hongcheng, Li Guideng
National Key Laboratory of Immunity and Inflammation, Suzhou Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Suzhou, Jiangsu, China.
Key Laboratory of Synthetic Biology Regulatory Elements, Suzhou Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Suzhou, Jiangsu, China.
PLoS Biol. 2025 Jul 14;23(7):e3003284. doi: 10.1371/journal.pbio.3003284. eCollection 2025 Jul.
Cancer cells and T cells engage in dynamic crosstalk within the tumor microenvironment (TME), shaping tumor progression and anti-tumor immunity. While cancer cells reprogram metabolism to support growth and immune evasion, T cells must adapt their metabolic states to maintain effector functions. Tumor-driven metabolic perturbations, such as nutrient depletion and accumulation of immunosuppressive metabolites, profoundly impair T cell function and fate. Conversely, metabolically reprogrammed T cells can modulate the TME and influence tumor growth. This reciprocal metabolic crosstalk represents both metabolic competition and intercellular communication, offering promising therapeutic targets.
癌细胞与T细胞在肿瘤微环境（TME）中进行动态串扰，影响肿瘤进展和抗肿瘤免疫。癌细胞通过重新编程代谢来支持生长和免疫逃逸，而T细胞必须调整其代谢状态以维持效应功能。肿瘤驱动的代谢紊乱，如营养物质耗竭和免疫抑制性代谢物的积累，会严重损害T细胞功能和命运。相反，代谢重编程的T细胞可以调节肿瘤微环境并影响肿瘤生长。这种相互的代谢串扰既代表了代谢竞争，也代表了细胞间通讯，提供了有前景的治疗靶点。
