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TRIM33 switches off Ifnb1 gene transcription during the late phase of macrophage activation

Federica Ferri1,2,3,4,5,6, Aude Parcelier1,2,3,4,5, Vanessa Petit1,2,3,4,5

  • 1CEA/DSV/iRCM/LRTS, 18 route du Panorama, Fontenay-aux-Roses 92265, France.

Nature Communications
|November 24, 2015
PubMed

Insights

TRIM33 protein is crucial for shutting down interferon-beta gene (Ifnb1) expression in macrophages after infection. Its deficiency leads to sustained Ifnb1 production, impacting the immune response.

Area of Science:

  • Immunology
  • Molecular Biology
  • Gene Regulation

Background:

  • The transcriptional regulation of interferon-beta (Ifnb1) is vital for innate immunity but not fully understood in activated macrophages.
  • Understanding Ifnb1 regulation is key to controlling viral and bacterial infections.

Purpose of the Study:

  • To elucidate the role of TRIM33 in the transcriptional regulation of Ifnb1 in macrophages.
  • To identify the mechanism by which TRIM33 controls Ifnb1 expression at late stages of immune activation.

Main Methods:

  • Investigated Ifnb1 expression in TRIM33-deficient macrophages and fibroblasts.
  • Utilized chromatin immunoprecipitation to assess TRIM33 binding to the Ifnb1 Control Element (ICE).
  • Analyzed enhanceosome loading and chromatin structure at the Ifnb1 locus.

Main Results:

  • TRIM33 deficiency caused sustained Ifnb1 expression in macrophages, but not fibroblasts, during toll-like receptor activation.
  • TRIM33 binds to the Ifnb1 Control Element (ICE) in macrophages, regulating enhanceosome assembly.
  • TRIM33 represses Ifnb1 transcription by inhibiting CBP/p300 recruitment to the gene.

Conclusions:

  • TRIM33 acts as a repressor of Ifnb1 transcription in macrophages.
  • Identified a novel mechanism of macrophage-specific Ifnb1 gene shutdown mediated by TRIM33.
  • TRIM33 is essential for terminating the inflammatory response by controlling Ifnb1 expression.

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