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Autophagy in infection, inflammation and immunity
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Autophagy in infection, inflammation and immunity
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Autophagy in infection, inflammation and immunity
Autophagy in infection, inflammation and immunity
Journal Article

Autophagy in infection, inflammation and immunity

2013
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Overview
Key Points 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. It is increasingly understood that autophagy is an ancient defence mechanism that has become incorporated into numerous immunological pathways. As discussed in this Review, its immunological roles include the elimination of microorganisms, the control of inflammation, the regulation of antigen presentation and lymphocyte homeostasis, and the secretion of immune mediators. Autophagy is a fundamental eukaryotic pathway that has multiple effects on immunity. Autophagy is induced by pattern recognition receptors and, through autophagic adaptors, it provides a mechanism for the elimination of intracellular microorganisms. Autophagy controls inflammation through regulatory interactions with innate immune signalling pathways, by removing endogenous inflammasome agonists and through effects on the secretion of immune mediators. Moreover, autophagy contributes to antigen presentation and to T cell homeostasis, and it affects T cell repertoires and polarization. Thus, as we discuss in this Review, autophagy has multitiered immunological functions that influence infection, inflammation and immunity.