期刊
CANCER DISCOVERY
卷 11, 期 7, 页码 1636-1643出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/2159-8290.CD-20-0569
关键词
-
类别
资金
- [F30 CA239367]
- [R01 CA217987]
- [R01 DK105550]
The metabolic reprogramming of T cells plays a crucial role in their function and fate, but is disrupted in cancer, potentially suppressing antitumor immunity. Therefore, stimulating effector T cell metabolism and enhancing cancer immunotherapy are challenges and opportunities that need to be addressed.
Immune oncology approaches of adoptive cell therapy and immune checkpoint blockade aim to activate T cells to eliminate tumors. Normal stimulation of resting T cells induces metabolic reprogramming from catabolic and oxidative metabolism to aerobic glycolysis in effector T cells, and back to oxidative metabolism in long-lived memory cells. These metabolic reprogramming events are now appreciated to be essential aspects of T-cell function and fate. Here, we review these transitions, how they are disrupted by T-cell interactions with tumors and the tumor microenvironment, and how they can inform immune oncology to enhance T-cell function against tumors. Significance: T-cell metabolism plays a central role in T-cell fate yet is altered in cancer in ways that can suppress antitumor immunity. Here, we discuss challenges and opportunities to stimulate effector T-cell metabolism and improve cancer immunotherapy.
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