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Links between autophagy, innate immunity, inflammation and Crohn's disease
1Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Albuquerque, NM 87131-001, USA. vderetic@salud.unm.edu
Abstract:
Autophagy is a fundamental biological process that endows eukaryotic cells with the ability to autodigest portions of their own cytoplasm. Autophagy plays roles in aging, development, neurodegeneration, cancer and immunity. The immunological role of autophagy was first recognized for the ability of autophagy to sanitize the cellular interior by killing intracellular microbes and, indirectly, by the adaptations that successful intracellular pathogens have evolved to protect themselves from autophagy. Since then, the repertoire of autophagy functions in immunity has been vastly expanded to include numerous intersections of regulatory and effector nature with innate and adaptive immunity. Autophagy acts both as an effector and a regulator of pattern recognition receptors, it supports MHC II presentation of cytosolic (self and microbial) antigens, it shapes central tolerance via thymic selection of the T cell repertoire, is an effector of Th1/Th2 polarization, affects homeostasis of T, B, and specialized immune cells such as Paneth cells, and - when defective - can be a contributing factor to chronic inflammatory conditions in human populations such as Crohn's disease.
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