Reprogramming of glutamine metabolism and its impact on immune response in the tumor microenvironment.
Reprogramming of glutamine metabolism and its impact on immune response in the tumor microenvironment.
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谷氨酰胺代谢重编程及其对肿瘤微环境中免疫反应的影响。
DOI：
10.1186/s12964-022-00909-0
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发表时间：
2022-07-27
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代谢重编程和免疫逃逸在肿瘤发生中起主要作用。越来越多的研究表明，谷氨酰胺代谢的重编程是肿瘤微环境（TME）中抗肿瘤免疫应答的假定决定因素。通常，肿瘤细胞在TME中对谷氨酰胺的掠夺性摄取导致免疫细胞对谷氨酰胺的有限利用，并影响抗肿瘤免疫应答。细胞程序性谷氨酰胺分配也影响抗肿瘤免疫应答。然而，肿瘤中谷氨酰胺代谢的重编程通过调节肿瘤PD-L1表达来调节免疫逃逸。同样，免疫细胞中谷氨酰胺代谢的重编程也会影响其免疫功能。此外，不同类型的谷氨酰胺代谢抑制剂广泛调节TME中的免疫细胞，同时抑制肿瘤细胞增殖。在此，我们讨论了肿瘤和免疫细胞的代谢重编程如何调节抗肿瘤免疫应答，以及在靶向肿瘤谷氨酰胺代谢的背景下不同免疫细胞的功能变化，这可以更好地解释靶向谷氨酰胺代谢与癌症免疫治疗相结合的潜力。视频摘要在线版本包含补充材料，可通过10. 1186/s12964-022-00909-0获取。
Metabolic reprogramming and immune escape play a major role in tumorigenesis. Increasing number of studies have shown that reprogramming of glutamine metabolism is a putative determinant of the anti-tumor immune response in the tumor microenvironment (TME). Usually, the predatory uptake of glutamine by tumor cells in the TME results in the limited utilization of glutamine by immune cells and affects the anti-tumor immune response. The cell-programmed glutamine partitioning also affects the anti-tumor immune response. However, the reprogramming of glutamine metabolism in tumors modulates immune escape by regulating tumor PD-L1 expression. Likewise, the reprogramming of glutamine metabolism in the immune cells also affects their immune function. Additionally, different types of glutamine metabolism inhibitors extensively regulate the immune cells in the TME while suppressing tumor cell proliferation. Herein, we discuss how metabolic reprogramming of tumor and immune cells regulates anti-tumor immune responses, as well as functional changes in different immune cells in the context of targeting tumor glutamine metabolism, which can better explain the potential of targeting glutamine metabolism in combination with immunotherapy for cancer. Video abstract The online version contains supplementary material available at 10.1186/s12964-022-00909-0.
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DOI：
10.1126/science.aac9935
发表时间：
2016-04-08
期刊：
Science (New York, N.Y.)
影响因子：
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作者：
Casey SC;Tong L;Li Y;Do R;Walz S;Fitzgerald KN;Gouw AM;Baylot V;Gütgemann I;Eilers M;Felsher DW
通讯作者：
Felsher DW
通过 mTOR 通路的代谢调节和抗血管生成利用 PD-L1 靶向共传递重塑肿瘤微环境
影响因子：
14
作者：
Chen, Binfan;Gao, Ang;Huang, Yongzhuo
通讯作者：
Huang, Yongzhuo
影响因子：
32.4
作者：
Blagih, Julianna;Coulombe, Francois;Jones, Russell G.
通讯作者：
Jones, Russell G.
影响因子：
5.6
作者：
CRAWFORD, J;COHEN, HJ
通讯作者：
COHEN, HJ
DOI：
10.1038/nrc.2016.71
发表时间：
2016-10
期刊：
Nature reviews. Cancer
影响因子：
--
作者：
Altman BJ;Stine ZE;Dang CV
通讯作者：
Dang CV