ArticleScience signaling2025
IRF1 cooperates with ISGF3 or GAF to form innate immune de novo enhancers in macrophages.
Article in Science signaling, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Review
- Multi-level transcriptional control of specific macrophage responses.The EMBO journal · 2026Review
- The Effects of Multiple Maillard Reaction Products in Infant Formula on Host Immunity and Neurotoxicity.Foods (Basel, Switzerland) · 2026Article
- Unraveling the layers of epigenetic control in respiratory antiviral defense.Journal of virology · 2026Review
- IFNγ-induced memory in human macrophages is sustained by the durability of cytokine signaling itself.The Journal of experimental medicine · 2026Article
- Dose-dependent IFN programs in myeloid cells after mRNA and adenovirus COVID-19 vaccination.JCI insight · 2026Article
- IFNγ shapes macrophage inflammatory responses by STAT1 isoform-specific epigenetic and transcriptional mechanisms.BMC genomics · 2026Article
- Rare epigenetic alterations are conserved across hematopoietic differentiation stages after mycobacterial infection.JCI insight · 2026Article
- Innate immune sensing and signaling: Co-opted for genome surveillance? Implications for tumorigenesis.DNA repair · 2025Review
- IFNγ-induced memory in human macrophages is not sustained by epigenetic changes but the durability of the cytokine itself.bioRxiv : the preprint server for biology · 2025Article
- Vascular smooth muscle cell-derived SOFrontiers in pharmacology · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Macrophages exposed to immune stimuli reprogram their epigenomes to alter their subsequent functions. Exposure to bacterial lipopolysaccharide (LPS) causes widespread nucleosome remodeling and the formation of thousands of de novo enhancers. We dissected the regulatory logic by which the network of interferon regulatory factors (IRFs) induces the opening of chromatin and the formation of de novo enhancers. We found that LPS-activated IRF3 mediated de novo enhancer formation indirectly by activating the type I interferon (IFN)-induced ISGF3. However, ISGF3 was generally needed to collaborate with IRF1, particularly where chromatin was less accessible. At these locations, IRF1 was required for the initial opening of chromatin, with ISGF3 extending accessibility and promoting the deposition of H3K4me1, marking poised enhancers. Because
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