Autophagy in inflammation, infection, and immunometabolism.


Journal

Immunity
ISSN: 1097-4180
Titre abrégé: Immunity
Pays: United States
ID NLM: 9432918

Informations de publication

Date de publication:
09 03 2021
Historique:
received: 13 11 2020
revised: 05 12 2020
accepted: 25 01 2021
entrez: 10 3 2021
pubmed: 11 3 2021
medline: 14 9 2021
Statut: ppublish

Résumé

Autophagy is a quality-control, metabolic, and innate immunity process. Normative autophagy affects many cell types, including hematopoietic as well as non-hematopoietic, and promotes health in model organisms and humans. When autophagy is perturbed, this has repercussions on diseases with inflammatory components, including infections, autoimmunity and cancer, metabolic disorders, neurodegeneration, and cardiovascular and liver diseases. As a cytoplasmic degradative pathway, autophagy protects from exogenous hazards, including infection, and from endogenous sources of inflammation, including molecular aggregates and damaged organelles. The focus of this review is on the role of autophagy in inflammation, including type I interferon responses and inflammasome outputs, from molecules to immune cells. A special emphasis is given to the intersections of autophagy with innate immunity, immunometabolism, and functions of organelles such as mitochondria and lysosomes that act as innate immunity and immunometabolic signaling platforms.

Identifiants

pubmed: 33691134
pii: S1074-7613(21)00041-8
doi: 10.1016/j.immuni.2021.01.018
pmc: PMC8026106
mid: NIHMS1668312
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

437-453

Subventions

Organisme : NIGMS NIH HHS
ID : P20 GM121176
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI111935
Pays : United States
Organisme : NIAID NIH HHS
ID : R37 AI042999
Pays : United States

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The author declares no competing interests.

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Auteurs

Vojo Deretic (V)

Autophagy Inflammation and Metabolism (AIM) Center of Biomedical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA; Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA. Electronic address: vderetic@salud.unm.edu.

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