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本文引用的文献

1
Disturbed mitochondrial dynamics in CD8 TILs reinforce T cell exhaustion.CD8 TIL 中受损的线粒体动力学增强了 T 细胞耗竭。
Nat Immunol. 2020 Dec;21(12):1540-1551. doi: 10.1038/s41590-020-0793-3. Epub 2020 Oct 5.
2
Cancer SLC43A2 alters T cell methionine metabolism and histone methylation.癌症 SLC43A2 改变 T 细胞蛋氨酸代谢和组蛋白甲基化。
Nature. 2020 Sep;585(7824):277-282. doi: 10.1038/s41586-020-2682-1. Epub 2020 Sep 2.
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IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression.IL4I1 是一种代谢免疫检查点,可激活 AHR 并促进肿瘤进展。
Cell. 2020 Sep 3;182(5):1252-1270.e34. doi: 10.1016/j.cell.2020.07.038. Epub 2020 Aug 19.
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Metabolic Modulation of Immunity: A New Concept in Cancer Immunotherapy.代谢免疫调节:癌症免疫治疗的新概念。
Cell Rep. 2020 Jul 7;32(1):107848. doi: 10.1016/j.celrep.2020.107848.
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Metabolism of immune cells in cancer.癌症中的免疫细胞代谢。
Nat Rev Cancer. 2020 Sep;20(9):516-531. doi: 10.1038/s41568-020-0273-y. Epub 2020 Jul 6.
6
Targeting glutamine metabolism enhances tumor-specific immunity by modulating suppressive myeloid cells.靶向谷氨酰胺代谢通过调节抑制性髓系细胞增强肿瘤特异性免疫。
J Clin Invest. 2020 Jul 1;130(7):3865-3884. doi: 10.1172/JCI131859.
7
Lactate dehydrogenase inhibition synergizes with IL-21 to promote CD8 T cell stemness and antitumor immunity.乳酸脱氢酶抑制与 IL-21 协同作用,促进 CD8 T 细胞干性和抗肿瘤免疫。
Proc Natl Acad Sci U S A. 2020 Mar 17;117(11):6047-6055. doi: 10.1073/pnas.1920413117. Epub 2020 Mar 2.
8
CD36-mediated metabolic adaptation supports regulatory T cell survival and function in tumors.CD36 介导的代谢适应支持调节性 T 细胞在肿瘤中的存活和功能。
Nat Immunol. 2020 Mar;21(3):298-308. doi: 10.1038/s41590-019-0589-5. Epub 2020 Feb 17.
9
Enhanced Lipid Accumulation and Metabolism Are Required for the Differentiation and Activation of Tumor-Associated Macrophages.增强脂质积累和代谢对于肿瘤相关巨噬细胞的分化和激活是必需的。
Cancer Res. 2020 Apr 1;80(7):1438-1450. doi: 10.1158/0008-5472.CAN-19-2994. Epub 2020 Feb 3.
10
Metabolic Profiling Using Stable Isotope Tracing Reveals Distinct Patterns of Glucose Utilization by Physiologically Activated CD8 T Cells.代谢谱分析利用稳定同位素示踪技术揭示了生理激活的 CD8 T 细胞对葡萄糖利用的不同模式。
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为免疫疗法助力:靶向代谢途径。

Fueling the Revolution: Targeting Metabolism to Enhance Immunotherapy.

机构信息

Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.

出版信息

Cancer Immunol Res. 2021 Mar;9(3):255-260. doi: 10.1158/2326-6066.CIR-20-0791.

DOI:10.1158/2326-6066.CIR-20-0791
PMID:33648947
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8240594/
Abstract

The success of immune-checkpoint blockade and chimeric antigen receptor (CAR) T cell therapies has established the remarkable capacity of the immune system to fight cancer. Over the past several years, it has become clear that immune cell responses to cancer are critically dependent upon metabolic programs that are specific to both immune cell type and function. Metabolic features of cancer cells and the tumor microenvironment impose constraints on immune cell metabolism that can favor immunosuppressive phenotypes and block antitumor responses. Advances in both preclinical and clinical studies have demonstrated that metabolic interventions can dramatically enhance the efficacy of immune-based therapies for cancer. As such, understanding the metabolic requirements of immune cells in the tumor microenvironment, as well as the limitations imposed therein, can have significant benefits for informing both current practice and future research in cancer immunotherapy.

摘要

免疫检查点阻断和嵌合抗原受体 (CAR) T 细胞疗法的成功确立了免疫系统对抗癌症的显著能力。在过去的几年中,人们已经清楚地认识到,免疫细胞对癌症的反应严重依赖于免疫细胞类型和功能特有的代谢程序。癌细胞和肿瘤微环境的代谢特征对免疫细胞代谢施加了限制,这些限制有利于免疫抑制表型并阻止抗肿瘤反应。临床前和临床研究的进展表明,代谢干预可以显著增强免疫疗法治疗癌症的疗效。因此,了解肿瘤微环境中免疫细胞的代谢需求以及其中的限制因素,对于为癌症免疫治疗的当前实践和未来研究提供信息具有重要意义。