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Autophagy in the regulation of pathogen replication and adaptive immunity


Randow, Felix; Münz, Christian (2012). Autophagy in the regulation of pathogen replication and adaptive immunity. Trends in Immunology, 33(10):475-87.

Abstract

Autophagy is an evolutionarily conserved homeostatic process by which cells deliver cytoplasmic material for degradation into lysosomes. Autophagy may have evolved as a nutrient-providing homeostatic pathway induced upon starvation, but with the acquisition of cargo receptors, autophagy has become an important cellular defence mechanism as well as a generator of antigenic peptides for major histocompatibility complex (MHC) presentation. We propose that autophagy efficiently protects against microbes encountering the cytosolic environment accidentally, for example, upon phagosomal damage, whereas pathogens routinely accessing the host cytosol have evolved to avoid or even benefit from autophagy.

Abstract

Autophagy is an evolutionarily conserved homeostatic process by which cells deliver cytoplasmic material for degradation into lysosomes. Autophagy may have evolved as a nutrient-providing homeostatic pathway induced upon starvation, but with the acquisition of cargo receptors, autophagy has become an important cellular defence mechanism as well as a generator of antigenic peptides for major histocompatibility complex (MHC) presentation. We propose that autophagy efficiently protects against microbes encountering the cytosolic environment accidentally, for example, upon phagosomal damage, whereas pathogens routinely accessing the host cytosol have evolved to avoid or even benefit from autophagy.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2012
Deposited On:18 Jan 2013 15:20
Last Modified:17 Feb 2018 00:37
Publisher:Elsevier
ISSN:1471-4906
OA Status:Green
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/j.it.2012.06.003
PubMed ID:22796170

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