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10.1089/jir.2016.0003

http://scihub22266oqcxt.onion/10.1089/jir.2016.0003
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suck abstract from ncbi


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pmid27379867
      J+Interferon+Cytokine+Res 2016 ; 36 (7 ): 454-61
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  • Epigenetic Mechanisms Governing Innate Inflammatory Responses #MMPMID27379867
  • Perkins DJ ; Patel MC ; Blanco JC ; Vogel SN
  • J Interferon Cytokine Res 2016[Jul]; 36 (7 ): 454-61 PMID27379867 show ga
  • 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.
  • |*Epigenesis, Genetic [MESH]
  • |*Gene Expression Regulation [MESH]
  • |Animals [MESH]
  • |Chromatin Assembly and Disassembly [MESH]
  • |Host-Pathogen Interactions/genetics/immunology [MESH]
  • |Humans [MESH]
  • |Immune Tolerance/genetics/immunology [MESH]
  • |Immunity, Innate/*genetics [MESH]
  • |Inflammation Mediators/metabolism [MESH]
  • |Inflammation/*genetics/*immunology/metabolism/microbiology [MESH]
  • |Interferons/metabolism [MESH]
  • |Jumonji Domain-Containing Histone Demethylases/metabolism [MESH]
  • |Macrophage Activation/genetics/immunology [MESH]
  • |Macrophages/immunology/metabolism [MESH]
  • |Promoter Regions, Genetic [MESH]


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