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Autophagy in the regulation of pathogen replication and adaptive immunity

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 a...

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Detalles Bibliográficos
Autores principales: Randow, Felix, Münz, Christian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Ltd. Published by Elsevier Ltd. 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3461100/
https://www.ncbi.nlm.nih.gov/pubmed/22796170
http://dx.doi.org/10.1016/j.it.2012.06.003
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author Randow, Felix
Münz, Christian
author_facet Randow, Felix
Münz, Christian
author_sort Randow, Felix
collection PubMed
description 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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spelling pubmed-34611002013-10-01 Autophagy in the regulation of pathogen replication and adaptive immunity Randow, Felix Münz, Christian Trends Immunol Article 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. Elsevier Ltd. Published by Elsevier Ltd. 2012-10 2012-07-14 /pmc/articles/PMC3461100/ /pubmed/22796170 http://dx.doi.org/10.1016/j.it.2012.06.003 Text en Copyright © 2012 Elsevier Ltd. Published by Elsevier Ltd. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Article
Randow, Felix
Münz, Christian
Autophagy in the regulation of pathogen replication and adaptive immunity
title Autophagy in the regulation of pathogen replication and adaptive immunity
title_full Autophagy in the regulation of pathogen replication and adaptive immunity
title_fullStr Autophagy in the regulation of pathogen replication and adaptive immunity
title_full_unstemmed Autophagy in the regulation of pathogen replication and adaptive immunity
title_short Autophagy in the regulation of pathogen replication and adaptive immunity
title_sort autophagy in the regulation of pathogen replication and adaptive immunity
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3461100/
https://www.ncbi.nlm.nih.gov/pubmed/22796170
http://dx.doi.org/10.1016/j.it.2012.06.003
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