Regulation and repurposing of nutrient sensing and autophagy in innate immunity

被引:42
|
作者
Sanchez-Garrido, Julia [1 ]
Shenoy, Avinash R. [1 ,2 ]
机构
[1] Imperial Coll London, Ctr Mol Bacteriol & Infect, Med Res Council, London SW7 2AZ, England
[2] Francis Crick Inst, London, England
基金
英国惠康基金; 英国医学研究理事会;
关键词
AMPK; immunity; LC3-associated phagocytosis; microbial pathogenesis; MTOR; unconventional secretion; MESSENGER-RNA TRANSLATION; ACTIVATED PROTEIN-KINASE; B-CELL ADAPTER; MYCOBACTERIUM-TUBERCULOSIS; LC3-ASSOCIATED PHAGOCYTOSIS; PARKINSONS-DISEASE; METABOLIC CHECKPOINT; BACTERIAL PATHOGENS; NEGATIVE REGULATION; SOMATIC MUTATIONS;
D O I
10.1080/15548627.2020.1783119
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Nutrients not only act as building blocks but also as signaling molecules. Nutrient-availability promotes cell growth and proliferation and suppresses catabolic processes, such as macroautophagy/autophagy. These effects are mediated by checkpoint kinases such as MTOR (mechanistic target of rapamycin kinase), which is activated by amino acids and growth factors, and AMP-activated protein kinase (AMPK), which is activated by low levels of glucose or ATP. These kinases have wide-ranging activities that can be co-opted by immune cells upon exposure to danger signals, cytokines or pathogens. Here, we discuss recent insight into the regulation and repurposing of nutrient-sensing responses by the innate immune system during infection. Moreover, we examine how natural mutations and pathogen-mediated interventions can alter the balance between anabolic and autophagic pathways leading to a breakdown in tissue homeostasis and/or host defense.
引用
收藏
页码:1571 / 1591
页数:21
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