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RTF1 mediates epigenetic control of Th17 cell differentiation via H2B monoubiquitination [CUT&RUN]

GSE269642 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2025/04/03 Platform GPL30172
Summary
The transcription factor RTF1 has been identified as a gene associated with an increased risk of ulcerative colitis (UC) . In this study, we investigated its impact on modulating intestinal inflammation through the control of T cells expressing interleukin-17A (Th17) cells. Our results demonstrate that RTF1 deficiency disrupts the differentiation of Th17 cells, while leaving regulatory T cells (Treg) cells unaffected. Mechanistically, RTF1 facilitates Histone H2B monoubiquitination (H2Bub1), which requires its histone modification domain (HMD). Impaired Th17 differentiation was also observed in cells lacking the H2Bub1 E3 ligase subunit RNF40. This study underscores the essential role of RTF1 in H2Bub1-mediated epigenetic regulation of Th17 cell differentiation. Understanding this process provides valuable insight into addressing Th17-associated inflammatory disorders.
Published in
RTF1 mediates epigenetic control of Th17 cell differentiation via H2B monoubiquitination
Galan C, Lu G, Gill R et al. · Journal of immunology (Baltimore, Md. : 1950) 2025 · PMID 40073106 · doi:10.1093/jimmun/vkae043
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Also filed as BioProject PRJNA1122923 and SRA study SRP513323. Searching any of these in the dataset finder brings you back here.

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