Histone deacetylase-2 controls IL-1β production through the regulation of NLRP3 expression and activation in tuberculosis infection
Jôsimar Dornelas Moreira, Alexei Iakhiaev, Ramakrishna Vankayalapati, Bock‐Gie Jung, Buka Samten
Abstract
-infected macrophages. These data suggest that HDAC2, but not HDAC1, controls IL-1β production through NLRP3 inflammasome activation, a mechanism with a significance in chronic inflammatory diseases including tuberculosis.
Topics & Concepts
HDAC1InflammasomeHistone deacetylase 2Histone deacetylaseHDAC4Mycobacterium tuberculosisGene knockdownHistoneChemistryHistone deacetylase 5InterleukinCell biologyTuberculosisCancer researchBiologyImmunologyCytokineMedicineBiochemistryInflammationGenePathologyHistone Deacetylase Inhibitors ResearchInflammasome and immune disordersNF-κB Signaling Pathways