ArticleCommunications biology2024
E4BP4 in macrophages induces an anti-inflammatory phenotype that ameliorates the severity of colitis.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Current Perspectives on the Inflammatory Bowel Disease Pathogenesis of Microbiota and the Gut-Brain Axis, and Emerging Therapeutics.Biomedicines · 2026Review
- Nfil3 integrates circadian rhythm and microbial metabolite signaling to maintain gut-liver immune-metabolic homeostasis under high-fat diet stress.Journal of translational medicine · 2026Article
- Multi-omics analysis identifies NFIL3 as a hypoxia-associated immune regulator in septic cardiomyopathy.Frontiers in immunology · 2026Article
- Disruption of the biorhythm in gastric epithelial cell triggers inflammation in Helicobacter pylori-associated gastritis by aberrantly regulating NFIL3 via CagA activated ERK-SP1 pathway.Cell communication and signaling : CCS · 2025Article
- Circadian Rhythm Dysregulation in Inflammatory Bowel Disease: Mechanisms and Chronotherapeutic Approaches.International journal of molecular sciences · 2025Review
- Loss of Cullin 5 in myeloid cells protects against autoimmune neuroinflammation.Frontiers in immunology · 2025Article
- The roles of output clock genes in regulating glucose metabolism.Journal of diabetes investigation · 2024Article
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Authors and funding
10 authors.
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Abstract
Macrophages are versatile cells of the innate immune system that work by altering their pro- or anti-inflammatory features. Their dysregulation leads to inflammatory disorders such as inflammatory bowel disease. We show that macrophage-specific upregulation of the clock output gene and transcription factor E4BP4 reduces the severity of colitis in mice. RNA-sequencing and single-cell analyses of macrophages revealed that increased expression of E4BP4 leads to an overall increase in expression of anti-inflammatory genes including Il4ra with a concomitant reduction in pro-inflammatory gene expression. In contrast, knockout of E4BP4 in macrophages leads to increased proinflammatory gene expression and decreased expression of anti-inflammatory genes. ChIP-seq and ATAC-seq analyses further identified Il4ra as a target of E4BP4, which drives anti-inflammatory polarization in macrophages. Together, these results reveal a critical role for E4BP4 in regulating macrophage inflammatory phenotypes and resolving inflammatory bowel diseases.
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