Autophagy in infection, inflammation and immunity

被引:0
|
作者
Vojo Deretic
Tatsuya Saitoh
Shizuo Akira
机构
[1] University of New Mexico Health Sciences Center,Department of Molecular Genetics and Microbiology
[2] Laboratory of Host Defense,undefined
[3] World Premier International Immunology Frontier Research Center,undefined
[4] Osaka University,undefined
来源
Nature Reviews Immunology | 2013年 / 13卷
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摘要
Autophagy is a fundamental eukaryotic homeostatic pathway that affects innate and adaptive immunity. Autophagic responses are integrated with pattern recognition receptor and cytokine signalling.Autophagic receptors, termed sequestosome 1-like receptors, target intracellular microorganisms for autophagy via ubiquitin and galectin tags, and they represent a new class of pattern recognition receptors. Intracellular pathogens have evolved elaborate strategies to prevent, neutralize or commandeer autophagy to support their own survival.Autophagy is a potent anti-inflammatory process that inhibits inflammasome activation and that modulates type I interferon responses. Autophagy affects the secretion of inflammatory and antimicrobial mediators.Autophagy enhances conventional phagosome maturation, affects antigen presentation, and influences T cell homeostasis and T helper cell polarization.Genetic predisposition and physiological links exist between autophagy and infectious, inflammatory and autoimmune diseases in humans.
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页码:722 / 737
页数:15
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