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代谢重编程诱导肿瘤微环境中巨噬细胞的极化。

Metabolic Reprogramming Induces Macrophage Polarization in the Tumor Microenvironment.

机构信息

Department of Laboratory Medicine, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.

Department of Radiology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.

出版信息

Front Immunol. 2022 Jul 7;13:840029. doi: 10.3389/fimmu.2022.840029. eCollection 2022.

Abstract

Macrophages are one of the most important cells in the innate immune system, they are converted into two distinct subtypes with completely different molecular phenotypes and functional features under different stimuli of the microenvironment: M1 macrophages induced by IFN-γ/lipopolysaccharides(LPS) and M2 macrophages induced by IL-4/IL-10/IL-13. Tumor-associated macrophages (TAMs) differentiate from macrophages through various factors in the tumor microenvironment (TME). TAMs have the phenotype and function of M2 macrophages and are capable of secreting multiple cytokines to promote tumor progression. Both tumor cells and macrophages can meet the energy needs for rapid cell growth and proliferation through metabolic reprogramming, so a comprehensive understanding of pro-tumor and antitumor metabolic switches in TAM is essential to understanding immune escape mechanisms. This paper focuses on the functions of relevant signaling pathways and cytokines during macrophage polarization and metabolic reprogramming, and briefly discusses the effects of different microenvironments and macrophage pathogenicity, in addition to describing the research progress of inhibitory drugs for certain metabolic and polarized signaling pathways.

摘要

巨噬细胞是先天免疫系统中最重要的细胞之一,在不同的微环境刺激下,它们可以转化为两种具有完全不同分子表型和功能特征的截然不同的亚型:IFN-γ/脂多糖(LPS)诱导的 M1 巨噬细胞和 IL-4/IL-10/IL-13 诱导的 M2 巨噬细胞。肿瘤相关巨噬细胞(TAMs)通过肿瘤微环境(TME)中的各种因素从巨噬细胞分化而来。TAMs 具有 M2 巨噬细胞的表型和功能,能够分泌多种细胞因子促进肿瘤进展。肿瘤细胞和巨噬细胞都可以通过代谢重编程满足快速细胞生长和增殖的能量需求,因此全面了解 TAM 中的促肿瘤和抗肿瘤代谢开关对于理解免疫逃逸机制至关重要。本文重点介绍了巨噬细胞极化和代谢重编程过程中相关信号通路和细胞因子的功能,并简要讨论了不同微环境和巨噬细胞致病性的影响,此外还描述了针对某些代谢和极化信号通路的抑制性药物的研究进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c39/9302576/a77ae3fea2ba/fimmu-13-840029-g001.jpg

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