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Targeting tumor metabolism to augment CD8+ T cell anti-tumor immunity

摘要CD8+T cell-based immune-therapeutics,including immune checkpoint inhibitors and adoptive cell therapies(tumor-infiltrating lymphocytes(TILs),T cell receptor-engineered T cells(TCR-T),chimeric antigen receptor T cells(CAR-T)),have achieved significant successes and prolonged patient survival to varying extents and even achieved cure in some cases.However,immunotherapy resistance and tumor insusceptibility frequently occur,leading to treatment failure.Recent evidences have highlighted the ponderance of tumor cells metabolic reprogramming in establishing an immunosuppressive milieu through the secretion of harmful metabolites,immune-inhibitory cytokines,and alteration of gene expression,which suppress the activity of immune cells,particularly CD8+T cells to evade immune surveillance.Therefore,targeting tumor cell metabolic adaptations to reshape the immune microenvi-ronment holds promise as an immunomodulatory strategy to facilitate immunotherapy.Here,we summarize recent advances in the crosstalk between immunotherapy and tumor reprogramming,focusing on the regulatory mechanisms underlying tumor cell glucose metabolism,amino acid meta-bolism,and lipid metabolism in influencing CD8+T cells to provide promising metabolic targets or combinational strategies for immunotherapy.

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作者 Huan Liu [1] Wenyong Yang [2] Jingwen Jiang [1] 学术成果认领
作者单位 West China School of Public Health and West China Fourth Hospital,Sichuan University,Frontiers Medical Center,Tianfu Jincheng Laboratory,Chengdu,610041,China;Department of Oncology,The First Affiliated Hospital of Xinxiang Medical University,Weihui,Henan,453100,China [1] Department of Neurosurgery,Medical Research Center,The Affiliated Hospital of Southwest Jiaotong University,The Second Chengdu Hospital Affiliated to Chongqing Medical University,The Third People's Hospital of Chengdu,Chengdu,610014,China [2]
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DOI 10.1016/j.jpha.2024.101150
发布时间 2025-09-30(万方平台首次上网日期,不代表论文的发表时间)
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药物分析学报(英文版)

药物分析学报(英文版)

2025年15卷5期

974-991页

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