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Despite its importance during viral or bacterial infections, transcriptional regulation of the interferon-β gene ( Ifnb1 ) in activated macrophages is only partially understood. Here we report that TRIM33 deficiency results in high, sustained expression of  Ifnb1  at late stages of toll-like receptor-mediated activation in macrophages but not in fibroblasts. In macrophages, TRIM33 is recruited by PU.1 to a conserved region, the  Ifnb1  Control Element (ICE), located 15 kb upstream of the  Ifnb1  transcription start site. ICE constitutively interacts with  Ifnb1  through a TRIM33-independent chromatin loop. At late phases of lipopolysaccharide activation of macrophages, TRIM33 is bound to ICE, regulates  Ifnb1  enhanceosome loading, controls  Ifnb1  chromatin structure and represses  Ifnb1  gene transcription by preventing recruitment of CBP/p300. These results characterize a previously unknown mechanism of macrophage-specific regulation of  Ifnb1  transcription whereby TRIM33 is critical for  Ifnb1  gene transcription shutdown.

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