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Autophagy in infection, inflammation and immunity
Open accessAbstract
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, 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]
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“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]
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“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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Metadata
- 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
- Venue
- Nature Reviews Immunology
- Published
- 2013-09-25
- Volume
- 13
- Issue
- 10
- Pages
- 722-737
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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