Suppression of T-cell responses by tumor metabolites

被引：70

作者：

Singer, Katrin ^{[1
]}

Gottfried, Eva ^{[2
]}

Kreutz, Marina ^{[2
]}

Mackensen, Andreas ^{[1
]}

机构：

[1] Univ Erlangen Nurnberg, Dept Internal Med Hematol Oncol 5, D-91054 Erlangen, Germany

[2] Univ Med Sch, Dept Hematol & Oncol, Regensburg, Germany

来源：

CANCER IMMUNOLOGY IMMUNOTHERAPY | 2011年 / 60卷 / 03期

关键词：

Tumor metabolism; Immune escape; Cytotoxic T cells; Lactic acid; HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; ACUTE LYMPHOBLASTIC-LEUKEMIA; L-ARGININE METABOLISM; INDOLEAMINE 2,3-DIOXYGENASE; GLUCOSE-METABOLISM; COLORECTAL-CANCER; PROGNOSTIC VALUE; LACTIC-ACID; ARGINASE-I; IFN-GAMMA;

D O I：

10.1007/s00262-010-0967-1

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Tumor cells have developed multiple mechanisms to escape T-cell-mediated immune recognition. Recent work has revealed that the altered tumor metabolism depletes essential nutrients or leads to the accumulation of immunosuppressive metabolites in the tumor microenvironment. In this review, we discuss the suppressive activity of some metabolic key players, which are upregulated in human tumor cells, including indolamine-2,3-dioxygenase (IDO), arginase, inducible nitric oxide synthetase (iNOS), and lactate dehydrogenase (LDH)-A, on the adaptive immune system. A better understanding of the impact of metabolic alterations of tumor cells on effector T-cell functions could lead to new therapeutic strategies to improve the efficacy of cancer immunotherapy.

引用

页码：425 / 431

页数：7

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