癌症代谢重编程被认为是肿瘤发生和抗肿瘤免疫反应中的一个新兴标志。与癌细胞一样，肿瘤微环境或转移前生态位内的免疫细胞也会经历广泛的代谢重编程，这深刻影响了抗肿瘤免疫反应。大量证据表明，免疫抑制性 TME 和肿瘤细胞释放的代谢物，包括乳酸、前列腺素 E2 (PGE2)、脂肪酸 (FAs)、胆固醇、D-2-羟基戊二酸 (2-HG)、腺苷 (ADO)、犬尿氨酸 (KYN) 可导致 CD8 T 细胞功能障碍。肿瘤细胞和免疫细胞之间这些代谢物的动态变化同样会引发 TME 中的代谢竞争，导致营养缺乏和随后的微环境酸中毒，从而阻碍免疫反应。这篇综述总结了肿瘤细胞经典代谢途径之外的新景观，强调了免疫抑制微环境中代谢紊乱的关键作用，特别是 TME 中的营养缺乏如何导致 CD8 T 细胞的代谢重编程。同样，它强调当前与肿瘤代谢和免疫反应相关的治疗靶点或策略，为未来的肿瘤免疫治疗和药物开发提供治疗益处。癌症代谢重编程被认为是肿瘤发生和抗肿瘤免疫反应中的一个新兴标志。肿瘤细胞和免疫细胞之间代谢物的动态变化引发 TME 中的代谢竞争，导致营养缺乏和随后的微环境酸中毒，从而阻碍免疫反应。© 2024。作者获得上海药物研究所独家许可，中国科学院、中国药理学会。

Cancer metabolic reprogramming has been considered an emerging hallmark in tumorigenesis and the antitumor immune response. Like cancer cells, immune cells within the tumor microenvironment or premetastatic niche also undergo extensive metabolic reprogramming, which profoundly impacts anti-tumor immune responses. Numerous evidence has illuminated that immunosuppressive TME and the metabolites released by tumor cells, including lactic acid, Prostaglandin E2 (PGE2), fatty acids (FAs), cholesterol, D-2-Hydroxyglutaric acid (2-HG), adenosine (ADO), and kynurenine (KYN) can contribute to CD8+ T cell dysfunction. Dynamic alterations of these metabolites between tumor cells and immune cells can similarly initiate metabolic competition in the TME, leading to nutrient deprivation and subsequent microenvironmental acidosis, which impedes immune response. This review summarizes the new landscape beyond the classical metabolic pathways in tumor cells, highlighting the pivotal role of metabolic disturbance in the immunosuppressive microenvironment, especially how nutrient deprivation in TME leads to metabolic reprogramming of CD8+ T cells. Likewise, it emphasizes the current therapeutic targets or strategies related to tumor metabolism and immune response, providing therapeutic benefits for tumor immunotherapy and drug development in the future. Cancer metabolic reprogramming has been considered an emerging hallmark in tumorigenesis and the antitumor immune response. Dynamic alterations of metabolites between tumor cells and immune cells initiate metabolic competition in the TME, leading to nutrient deprivation and subsequent microenvironmental acidosis, which impedes immune response.© 2024. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.