Energy metabolism manipulates the fate and function of tumour myeloid-derived suppressor cells

被引:53
|
作者
Hu, Cong [1 ,2 ,3 ]
Pang, Bo [1 ,4 ]
Lin, Guangzhu [4 ]
Zhen, Yu [5 ]
Yi, Huanfa [1 ,2 ]
机构
[1] First Hosp Jilin Univ, Cent Lab, Changchun 130031, Jilin, Peoples R China
[2] Minist Educ, Key Lab Organ Regenerat & Transplantat, Changchun 130021, Jilin, Peoples R China
[3] First Hosp Jilin Univ, Ctr Prenatal Diag, Ctr Reprod Med, Changchun 130021, Jilin, Peoples R China
[4] First Hosp Jilin Univ, Dept Cardiol, Changchun 130031, Jilin, Peoples R China
[5] First Hosp Jilin Univ, Dept Dermatol, Changchun 130021, Jilin, Peoples R China
基金
中国国家自然科学基金;
关键词
NITRIC-OXIDE SYNTHASE; IMMUNE SUPPRESSION; ACID-TRANSPORT; T-CELLS; ARGININE; CANCER; EXPRESSION; RESPONSES; IDO; DIFFERENTIATION;
D O I
10.1038/s41416-019-0644-x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
In recent years, a large number of studies have been carried out in the field of immune metabolism, highlighting the role of metabolic energy reprogramming in altering the function of immune cells. Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of cells generated during a large array of pathological conditions, such as cancer, inflammation, and infection, and show remarkable ability to suppress T-cell responses. These cells can also change their metabolic pathways in response to various pathogen-derived or inflammatory signals. In this review, we focus on the roles of glucose, fatty acid (FA), and amino acid (AA) metabolism in the differentiation and function of MDSCs in the tumour microenvironment, highlighting their potential as targets to inhibit tumour growth and enhance tumour immune surveillance by the host. We further highlight the remaining gaps in knowledge concerning the mechanisms determining the plasticity of MDSCs in different environments and their specific responses in the tumour environment. Therefore, this review should motivate further research in the field of metabolomics to identify the metabolic pathways driving the enhancement of MDSCs in order to effectively target their ability to promote tumour development and progression.
引用
收藏
页码:23 / 29
页数:7
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