Epigenetic Mechanisms Governing Innate Inflammatory Responses

J Interferon Cytokine Res. 2016 Jul;36(7):454-61. doi: 10.1089/jir.2016.0003.

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

  • Review
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Chromatin Assembly and Disassembly
  • Epigenesis, Genetic*
  • Gene Expression Regulation*
  • Host-Pathogen Interactions / genetics
  • Host-Pathogen Interactions / immunology
  • Humans
  • Immune Tolerance / genetics
  • Immune Tolerance / immunology
  • Immunity, Innate / genetics*
  • Inflammation / genetics*
  • Inflammation / immunology*
  • Inflammation / metabolism
  • Inflammation / microbiology
  • Inflammation Mediators / metabolism
  • Interferons / metabolism
  • Jumonji Domain-Containing Histone Demethylases / metabolism
  • Macrophage Activation / genetics
  • Macrophage Activation / immunology
  • Macrophages / immunology
  • Macrophages / metabolism
  • Promoter Regions, Genetic
  • Toll-Like Receptors / metabolism

Substances

  • Inflammation Mediators
  • Toll-Like Receptors
  • Interferons
  • Jumonji Domain-Containing Histone Demethylases