Epigenetic Mechanisms Governing Innate Inflammatory Responses
Open accessAbstract
Toll-like receptors (TLRs) are major receptors of the host innate immune system that recognize conserved pathogen-associated molecular patterns (PAMPs) of invading microbes. Activation of TLR signaling culminates in the expression of multiple genes in a coordinate and kinetically defined manner. In this review, we summarize the current studies describing the chromatin landscape of TLR-responsive inflammatory genes and how changes to this chromatin landscape govern cell type-specific and temporal gene expression. We further elaborate classical endotoxin tolerance and epigenetic mechanisms controlling tolerance and interferon priming effects on inflammatory promoters.
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Epigenetic changes may alter cell type-specific and temporal gene expression, ultimately altering individual patient risk for fungal infections.
“The epigenetic changes may alter cell type-specific and temporal gene expression ultimately resulting alterations of individual patient risk for fungal infections [49].”
From Race and ethnicity: Risk factors for fungal infections? (2023) · cites this paper as [49]
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References 63 · Cited by 51
- Authors
- Perkins, D. J., Patel, M. C., Blanco, J. C. G., & Vogel, S. N.
- Affiliations
- University of Maryland, Baltimore (US)
- Sigmovir Biosystems (United States) (US)
- Corresponding author
- Vogel, Stefanie N.
- Venue
- Journal of Interferon & Cytokine Research
- Publisher
- SAGE Publications
- Published
- 2016-07
- Volume
- 36
- Issue
- 7
- Pages
- 454-461
- ISSN
- 1079-9907 (ISSN-L)
- 1557-7465
- PMC
- PMC4931723
- OpenAlex
- W2472138123
- Cited by
- 51
- References
- 63
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 7 · 2023: 7 · 2022: 14 · 2021: 3 · 2020: 4 · 2019: 5 · 2018: 4 · 2017: 3 · 2016: 2
- FWCI
- 0.45
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Interferon & Cytokine Research (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AI18797)
- National Institute of Allergy and Infectious Diseases (R56AI018797, R01AI123371, R01AI104541)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- Toll-like receptors, epigenetic regulation, innate immunity, inflammatory gene expression, chromatin landscape, endotoxin tolerance, interferon priming, pathogen-associated molecular patterns, cell type-specific gene expression, temporal gene expression
- MeSH terms
- Animals, Gene Expression Regulation, Humans, Immune Tolerance, Immunity, Innate, Inflammation, Interferons, Macrophage Activation, Macrophages, Promoter Regions, Genetic, Inflammation Mediators, Chromatin Assembly and Disassembly, Epigenesis, Genetic, Toll-Like Receptors, Host-Pathogen Interactions, Jumonji Domain-Containing Histone Demethylases
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