Cytoplasmic Mechanisms of Recognition and Defense of Microbial Nucleic Acids
Open accessAbstract
Microbial nucleic acids are major signatures of invading pathogens, and their recognition by various host pattern recognition receptors (PRRs) represents the first step toward an efficient innate immune response to clear the pathogens. The nucleic acid–sensing PRRs are localized at the plasma membrane, the cytosol, and/or various cellular organelles. Sensing of nucleic acids and signaling by PRRs involve recruitment of distinct signaling components, and PRRs are intensively regulated by cellular organelle trafficking. PRR-mediated innate immune responses are also heavily regulated by posttranslational modifications, including phosphorylation, polyubiquitination, sumoylation, and glutamylation. In this review, we focus on our current understanding of recognition of microbial nucleic acid by PRRs, particularly on their regulation by organelle trafficking and posttranslational modifications. We also discuss how sensing of self nucleic acids and dysregulation of PRR-mediated signaling lead to serious human diseases.
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The interaction of dECM scaffolds with the innate immune system is mainly mediated via DAMPs, danger signals released upon cell and ECM damage during graft processing or implantation.
“The interaction of dECM scaffolds with the innate immune system is mainly mediated via damage-associated molecular patterns (DAMPs), danger signals released upon the cell and ECM damage during graft processing or implantation.”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [37]
Nuclear and mitochondrial DNA, ROS, and fragmented ECM components such as hyaluronic acid or fibronectin are among the most renowned DAMPs.
“Nuclear and mitochondrial DNA, reactive oxygen species (ROS), and fragmented ECM components such as hyaluronic acid or fibronectin are among the most renowned DAMPs, which are released due to perturbation in the arrangement of nucleic acids within cells, transplantation imperfections such as ischemia-reperfusion, and harsh decellularization strategies, respectively [34–37].”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [37]
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GPAT4 regulates antitumor immune response through activating the mtDNA-cGAS axis in cancer cells
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Self-citationSTRAP upregulates antiviral innate immunity against PRV by targeting TBK1
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FBXW7 is a multifaceted regulator of the innate immune response to DNA viruses
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Self-citation
- Authors
- Hu, M.-M., & Shu, H.-B.
- Affiliations
- Wuhan University (CN)
- Venue
- Annual Review of Cell and Developmental Biology
- Publisher
- Annual Reviews
- Published
- 2018-10-06
- Volume
- 34
- Issue
- 1
- Pages
- 357-379
- ISSN
- 1081-0706 (ISSN-L)
- 1530-8995
- OpenAlex
- W2887534894
- Cited by
- 110
- References
- 163
- Citations by year
- 2026: 6 · 2025: 19 · 2024: 8 · 2023: 13 · 2022: 23 · 2021: 10 · 2020: 15 · 2019: 14 · 2018: 2
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Cell and Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31521091, 31630045)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- pattern recognition receptors, innate immunity, organelle trafficking, post-translational modification, phosphorylation, polyubiquitination, SUMOylation, glutamylation, host-pathogen recognition
- MeSH terms
- Bacteria, Cytoplasm, DNA, Bacterial, Humans, Immunity, Innate, Nucleic Acids, Protein Processing, Post-Translational, Signal Transduction, Receptors, Pattern Recognition, Host-Pathogen Interactions
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