Abstract
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.
Publication types
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Review
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Chromatin Assembly and Disassembly
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Epigenesis, Genetic*
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Gene Expression Regulation*
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Host-Pathogen Interactions / genetics
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Host-Pathogen Interactions / immunology
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Humans
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Immune Tolerance / genetics
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Immune Tolerance / immunology
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Immunity, Innate / genetics*
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Inflammation / genetics*
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Inflammation / immunology*
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Inflammation / metabolism
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Inflammation / microbiology
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Inflammation Mediators / metabolism
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Interferons / metabolism
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Jumonji Domain-Containing Histone Demethylases / metabolism
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Macrophage Activation / genetics
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Macrophage Activation / immunology
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Macrophages / immunology
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Macrophages / metabolism
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Promoter Regions, Genetic
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Toll-Like Receptors / metabolism
Substances
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Inflammation Mediators
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Toll-Like Receptors
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Interferons
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Jumonji Domain-Containing Histone Demethylases