Autophagy in infection, inflammation and immunity

Deretic, Vojo; Saitoh, Tatsuya; Akira, Shizuo

doi:10.1038/nri3532

Cited by 1,919Autophagy in Disease and TherapyImmune Response and InflammationPhagocytosis and Immune Regulation

Autophagy in infection, inflammation and immunity

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Deretic, Vojo, Saitoh, Tatsuya, Akira, Shizuo·2013·Nature Reviews Immunology

DOI 10.1038/nri3532PMC PMC5340150

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Abstract

Autophagy is a fundamental eukaryotic pathway that has multiple effects on immunity. Autophagy is induced by pattern recognition receptors and, through autophagic adaptors, it provides a mechanism for the elimination of intracellular microorganisms. Autophagy controls inflammation through regulatory interactions with innate immune signalling pathways, by removing endogenous inflammasome agonists and through effects on the secretion of immune mediators. Moreover, autophagy contributes to antigen presentation and to T cell homeostasis, and it affects T cell repertoires and polarization. Thus, as we discuss in this Review, autophagy has multitiered immunological functions that influence infection, inflammation and immunity.

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Activated macrophages can use macro-autophagy to eliminate intracellular bacteria such as L. monocytogenes, Shigella spp., and M. tuberculosis.
“Activated macrophages can use macro-autophagy, the cellular intrinsic degradation and recycling system for senescent organelles and compartments, to eliminate intracellular bacteria such as L. monocytogenes, Shigella spp., and M. tuberculosis (55).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [55]
In a downstream conjugation cascade, the Atg5/Atg12/Atg16 complex supports linking LC3s to membrane phosphoethanolamine.
“In a downstream conjugation cascade, the Atg5/Atg12/Atg16 complex supports linking LC3s to membrane phosphoethanolamine (55).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [55]
Activated macrophages can limit growth of intracellular bacteria including M. tuberculosis and drive phagosome maturation toward phagolysosomes and auto-phagolysosomes.
“Activated MΦs can limit growth of intracellular bacteria including M. tuberculosis and drive phagosome maturation toward phagolysosomes and auto-phagolysosomes (54, 55).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [55]

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Authors: Deretic, V., Saitoh, T., & Akira, S.
Affiliations: University of New Mexico (US)
Immunology Frontier Research Center, The University of Osaka (JP)
Corresponding author: Deretic, Vojo
ORCID: Deretic, Vojo
Akira, Shizuo
Venue: Nature Reviews Immunology
Publisher: Springer Science and Business Media LLC
Published: 2013-09-25
Volume: 13
Issue: 10
Pages: 722-737
ISSN: 1474-1733 (ISSN-L)
1474-1741
DOI: 10.1038/nri3532
PMC: PMC5340150
OpenAlex: W2148281700
Cited by: 1,919
References: 151
Citations by year: 2026: 104 · 2025: 97 · 2024: 116 · 2023: 150 · 2022: 151 · 2021: 179 · 2020: 179 · 2019: 174 · 2018: 170 · 2017: 185 · 2016: 173 · 2015: 129 · 2014: 107 · 2013: 4
FWCI: 16.31
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Immunology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (UL1TR000041, UL1TR001449)
National Institute of Allergy and Infectious Diseases (R01AI045148, AI042999)
National Center for Advancing Translational Sciences
Topics: Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Keywords: autophagy, infection, inflammation, immunity, pattern recognition receptors, innate immune signaling, inflammasome, antigen presentation, T cell homeostasis, T cell polarization, T cell receptor repertoire
MeSH terms: Autophagy, Bacterial Infections, Gene Expression Regulation, Homeostasis, Humans, Immunity, Innate, Inflammation, T-Lymphocytes, Virus Diseases, Signal Transduction, Antigen Presentation, Protein Transport, Adaptor Proteins, Signal Transducing, Receptors, Pattern Recognition, Inflammasomes

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