Cell Intrinsic and Systemic Metabolism in Tumor Immunity and Immunotherapy

被引：17

作者：

Coleman, Michael F. ^{[1
]}

Cozzo, Alyssa J. ^{[1
,2
]}

Pfeil, Alexander J. ^{[1
]}

Etigunta, Suhas K. ^{[1
]}

Hursting, Stephen D. ^{[1
,3
]}

机构：

[1] Univ N Carolina, Dept Nutr, Chapel Hill, NC 27516 USA

[2] Duke Univ, Dept Med, Durham, NC 27705 USA

[3] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27516 USA

来源：

CANCERS | 2020年 / 12卷 / 04期

关键词：

immune checkpoint inhibition; metabolism; cancer; obesity; calorie restriction; HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; MHC CLASS-I; LACTIC-ACID; CALORIC RESTRICTION; T-CELLS; B-CELLS; INFILTRATING CD4(+); GLUCOSE-METABOLISM; ANTITUMOR IMMUNITY; SUPPRESSOR-CELLS;

D O I：

10.3390/cancers12040852

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Immune checkpoint inhibitor (ICI) therapy has shown extraordinary promise at treating cancers otherwise resistant to treatment. However, for ICI therapy to be effective, it must overcome the metabolic limitations of the tumor microenvironment. Tumor metabolism has long been understood to be highly dysregulated, with potent immunosuppressive effects. Moreover, T cell activation and longevity within the tumor microenvironment are intimately tied to T cell metabolism and are required for the long-term efficacy of ICI therapy. We discuss in this review the intersection of metabolic competition in the tumor microenvironment, T cell activation and metabolism, the roles of tumor cell metabolism in immune evasion, and the impact of host metabolism in determining immune surveillance and ICI therapy outcomes. We also discussed the effects of obesity and calorie restriction-two important systemic metabolic perturbations that impact intrinsic metabolic pathways in T cells as well as cancer cells.

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