Metabolism and macrophages in the tumor microenvironment

被引:0
|
作者
Yang, Hannah [1 ,2 ,3 ]
Kim, Chan [1 ,2 ,3 ]
Zou, Weiping [1 ,2 ,4 ,5 ]
机构
[1] Univ Michigan, Sch Med, Dept Surg, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Sch Med, Ctr Excellence Canc Immunol & Immunotherapy, Rogel Canc Ctr, Ann Arbor, MI 48109 USA
[3] CHA Univ, Med Oncol, Sch Med, Seongnam, South Korea
[4] Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA
[5] Univ Michigan, Sch Med, Grad Programs Canc Biol & Immunol, Ann Arbor, MI 48109 USA
基金
美国国家卫生研究院; 新加坡国家研究基金会;
关键词
CANCER MICROENVIRONMENT; TREM2; ACCUMULATION; ACTIVATION; EXPRESSION; PI3K-GAMMA; IL-1-BETA; INHIBITOR; SECRETION; SUCCINATE;
D O I
10.1016/j.coi.2024.102491
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Tumor-associated macrophages (TAMs) constitute the primary subset of immune cells within the tumor microenvironment (TME). Exhibiting both phenotypic and functional heterogeneity, TAMs play distinct roles in tumor initiation, progression, and responses to therapy in patients with cancer. In response to various immune and metabolic cues within the TME, TAMs dynamically alter their metabolic profiles to adapt. Changes in glucose, amino acid, and lipid metabolism in TAMs, as well as their interaction with oncometabolites, not only sustain their energy demands but also influence their impact on tumor immune responses. Understanding the molecular mechanisms underlying the metabolic reprogramming of TAMs and their orchestration of metabolic processes can offer insights for the development of novel cancer immunotherapies targeting TAMs. Here, we discuss how metabolism reprograms macrophages in the TME and review clinical trials aiming to normalize metabolic alterations in TAMs and alleviate TAM-mediated immune suppression and protumor activity.
引用
收藏
页数:10
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