title: Logic of the inflammation-associated transcriptional response.
abstract: Immune response to pathogens depends on coordinated regulation of numerous genes that contribute collectively to pathogen elimination and restoration of the integrity of the affected tissue. The pathogen-induced gene expression is governed largely by the signal-induced posttranslational histone modifications that facilitate assembly of the functionally distinct chromatin complexes. In this review, we describe the principles of chromatin-based gene regulation during innate immune responses. We discuss the ability of pathogens to hijack the host response by interfering with various arms of transcriptional machinery involved in the responses. In particular, we discuss the phenomenon of the histone mimicry where interaction between histones and transcriptional regulators is targeted by pathogens that carry the histone-like sequences (histone mimics). We show how the principle of isotone mimicry as an efficient way to control host gene expression has been sued for the development of novel anti-inflammatory pharmacological approaches.
authors.affiliation: Rockefeller University, New York, New York, USA. tarakho@mail.rockefeller.edu
authors.forename: Alexander
authors.initials: A
authors.lastname: Tarakhovsky
mesh_terms: D002843:Chromatin / Q000378:metabolism; D005786:Gene Expression Regulation; D006657:Histones / Q000235:genetics / Q000276:immunology; D054884:Host-Pathogen Interactions / Q000276:immunology*; D006801:Humans; D057131:Immune Evasion / Q000276:immunology*; D007113:Immunity, Innate; D007249:Inflammation / Q000235:genetics* / Q000276:immunology*; D012326:RNA Splicing; D014158:Transcription, Genetic
chemical_list: D002843:Chromatin; D006657:Histones
keywords: Bromodomain inhibitor; Chromatin; Epigenetics; Gene expression; Histone; Immune response; Inflammation; Pathogen