Intracellular recognition of pathogens and autophagy as an innate immune host defence
Open accessAbstract
Pathogen recognition is the first and crucial step in innate immunity. Molecular families involved in the recognition of pathogens and activation of the innate immune responses in immunoreactive cells include the Toll-like receptor family in mammals and the peptidoglycan recognition protein (PGRP) family in Drosophila, which sense microorganisms in an extracellular or luminal compartment. Other emerging families are the intracellular recognition molecules for bacteria, such as nucleotide binding and oligomerization domain-like receptors in mammals and PGRP--LE in Drosophila, several of which have been shown to detect structures of bacterial peptidoglycan in the host cell cytosol. Exciting advances in recent studies on autophagy indicate that macroautophagy (referred to here as autophagy) is selectively induced by intracellular recognition molecules and has a crucial role in the elimination of intracellular pathogens, including bacteria, viruses and parasites. This review discusses recent studies related to intracellular recognition molecules and innate immune responses to intracellular pathogens, and highlights the role of autophagy in innate immunity.
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The autophagic machinery following pathogen entry into cells can target either bacteria-containing phagosomes or free cytosolic bacteria.
“The autophagic machinery following the entry of the pathogen into cells can target either bacteria-containing phagosomes, or free cytosolic bacteria [8,9,10,11].”
From LC3-Associated Phagocytosis (LAP): Connections with Host Autophagy (2012) · cites this paper as [10]
Cites
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Induction of autophagy supports the bioenergetic demands of quiescent muscle stem cell activation
Tang, A. H., & Rando, T. A. (2014) · The EMBO Journal · doi:10.15252/embj.201488278 · Cited by 294 · see citing works
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- Authors
- Yano, T., & Kurata, S.
- Affiliations
- Tohoku University (JP)
- ORCID
- Venue
- Journal of Biochemistry
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-07-05
- Volume
- 150
- Issue
- 2
- Pages
- 143-149
- ISSN
- 0021-924X (ISSN-L)
- PMC
- PMC3202912
- OpenAlex
- W1966342688
- Cited by
- 54
- References
- 4
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 4 · 2021: 2 · 2020: 3 · 2018: 4 · 2017: 5 · 2016: 5 · 2015: 7 · 2014: 4 · 2013: 8 · 2012: 8
- FWCI
- 0.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Biochemistry (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Japan Society for the Promotion of Science
- National Institute of Allergy and Infectious Diseases (AI07495)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Invertebrate Immune Response Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- autophagy, innate immunity, peptidoglycan recognition proteins, NOD-like receptors, Toll-like receptors, peptidoglycan sensing, selective autophagy, intracellular bacteria
- MeSH terms
- Animals, Autophagy, Carrier Proteins, Humans, Immunity, Innate, Inflammation, Insecta, Virus Physiological Phenomena, Bacterial Physiological Phenomena, Toll-Like Receptors, Nod Signaling Adaptor Proteins, Host-Pathogen Interactions
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