巨噬细胞
先天免疫系统
生物
细胞生物学
免疫系统
线粒体
炎症
细胞内寄生虫
微生物学
促炎细胞因子
细胞因子
吞噬作用
病菌
免疫学
脂多糖
作者
Subhadip Choudhuri,Imran H. Chowdhury,Nisha Jain Garg
标识
DOI:10.3389/fimmu.2020.622602
摘要
Innate immune cells play the first line of defense against pathogens. Phagocytosis or invasion by pathogens can affect mitochondrial metabolism in macrophages by diverse mechanisms and shape the macrophage response (proinflammatory vs. immunomodulatory) against pathogens. Besides β-nicotinamide adenine dinucleotide 2'-phosphate, reduced (NADPH) oxidase, mitochondrial electron transport chain complexes release superoxide for direct killing of the pathogen. Mitochondria that are injured are removed by mitophagy, and this process can be critical for regulating macrophage activation. For example, impaired mitophagy can result in cytosolic leakage of mitochondrial DNA (mtDNA) that can lead to activation of cGAS-STING signaling pathway of macrophage proinflammatory response. In this review, we will discuss how metabolism, mtDNA, mitophagy, and cGAS-STING pathway shape the macrophage response to infectious agents.
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