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The molecular regulation of autophagy in antimicrobial immunity
Autophagy is a catabolic process that can degrade worn-out organelles and invading pathogens. The activation of autophagy regulates innate and adaptive immunity, playing a key role in the response to microbial invasion. Microbial infection may cause different consequences such as the elimination of...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9335221/ https://www.ncbi.nlm.nih.gov/pubmed/35278083 http://dx.doi.org/10.1093/jmcb/mjac015 |
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author | Qin, Chuan Lu, Yalan Bai, Lin Wang, Kewei |
author_facet | Qin, Chuan Lu, Yalan Bai, Lin Wang, Kewei |
author_sort | Qin, Chuan |
collection | PubMed |
description | Autophagy is a catabolic process that can degrade worn-out organelles and invading pathogens. The activation of autophagy regulates innate and adaptive immunity, playing a key role in the response to microbial invasion. Microbial infection may cause different consequences such as the elimination of invaders through autophagy or xenophagy, host cell death, and symbiotic relationships. Pathogens adapt to the autophagy mechanism and further relieve intracellular stress, which is conducive to host cell survival and microbial growth. The regulation of autophagy forms a complex network through which host immunity is modulated, resulting in a variety of pathophysiological manifestations. Modification of the autophagic pathway is an essential target for the development of antimicrobial drugs. |
format | Online Article Text |
id | pubmed-9335221 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-93352212022-07-29 The molecular regulation of autophagy in antimicrobial immunity Qin, Chuan Lu, Yalan Bai, Lin Wang, Kewei J Mol Cell Biol Review Autophagy is a catabolic process that can degrade worn-out organelles and invading pathogens. The activation of autophagy regulates innate and adaptive immunity, playing a key role in the response to microbial invasion. Microbial infection may cause different consequences such as the elimination of invaders through autophagy or xenophagy, host cell death, and symbiotic relationships. Pathogens adapt to the autophagy mechanism and further relieve intracellular stress, which is conducive to host cell survival and microbial growth. The regulation of autophagy forms a complex network through which host immunity is modulated, resulting in a variety of pathophysiological manifestations. Modification of the autophagic pathway is an essential target for the development of antimicrobial drugs. Oxford University Press 2022-03-12 /pmc/articles/PMC9335221/ /pubmed/35278083 http://dx.doi.org/10.1093/jmcb/mjac015 Text en © The Author(s) (2022). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, CEMCS, CAS. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Qin, Chuan Lu, Yalan Bai, Lin Wang, Kewei The molecular regulation of autophagy in antimicrobial immunity |
title | The molecular regulation of autophagy in antimicrobial immunity |
title_full | The molecular regulation of autophagy in antimicrobial immunity |
title_fullStr | The molecular regulation of autophagy in antimicrobial immunity |
title_full_unstemmed | The molecular regulation of autophagy in antimicrobial immunity |
title_short | The molecular regulation of autophagy in antimicrobial immunity |
title_sort | molecular regulation of autophagy in antimicrobial immunity |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9335221/ https://www.ncbi.nlm.nih.gov/pubmed/35278083 http://dx.doi.org/10.1093/jmcb/mjac015 |
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