ArticleThe Journal of clinical investigation2021
BMI1 maintains the Treg epigenomic landscape to prevent inflammatory bowel disease.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The trial behind it
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Next-Generation regulatory T cell therapies: Translational considerations for inflammatory bowel disease.Human immunology · 2026Review
- Article
- Th17/treg balance in Inflammatory Bowel Disease: the role of microbial, and genetic regulators in disease modulation.Frontiers in cell and developmental biology · 2026Review
- Pannexin-1 hemichannels promote experimental colitis inflammation in a CD4Frontiers in immunology · 2025Article
- TGF-β1-triggered BMI1 and SMAD2 cooperatively regulate miR-191 to modulate bone formation.Molecular therapy. Nucleic acids · 2024Article
- The FOXP3Gastroenterology · 2024Article
- Epigenetics of Inflammatory Bowel Diseases.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Article
- G9a Modulates Lipid Metabolism in CD4 T Cells to Regulate Intestinal Inflammation.Gastroenterology · 2023Article
- Multi-omics in Crohn's disease: New insights from inside.Computational and structural biotechnology journal · 2023Review
- Epigenetic modulations of immune cells: from normal development to tumor progression.International journal of biological sciences · 2023Review
- Cell Type-Specific Induction of Inflammation-Associated Genes in Crohn's Disease and Colorectal Cancer.International journal of molecular sciences · 2022Article
- Nature vs. nurture: FOXP3, genetics, and tissue environment shape Treg function.Frontiers in immunology · 2022Review
- Nuclear Coregulatory Complexes in Tregs as Targets to Promote Anticancer Immune Responses.Frontiers in immunology · 2022Review
- Review
- Myeloid-Derived Suppressor Cells Alleviate Renal Fibrosis ProgressionFrontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 2 countries.
Funding
Abstract
FOXP3+ Tregs are expanded within the inflamed intestine of human Crohn's disease, yet FOXP3-mediated gene repression within these cells is lost. The polycomb repressive complexes play a role in FOXP3 target gene regulation, but deeper mechanistic insight is incomplete. We have now specifically identified the polycomb-repressive complex 1 (PRC1) family member, BMI1 in the regulation of a proinflammatory enhancer network in both human and murine Tregs. Using human Tregs and lamina propria T cells, we inferred PRC1 to regulate Crohn's associated gene networks through assays of chromatin accessibility. Conditional deletion of BMI1 in murine FOXP3+ cells led to systemic inflammation. BMI1-deficient Tregs beared a TH1/TH17-like phenotype as assessed by assays of genome wide transcription, chromatin accessibility and proteomic techniques. Finally, BMI1 mutant FOXP3+ cells did not suppress colitis in the adoptive transfer model of human inflammatory bowel disease. We propose that BMI1 plays an important role in enforcing Treg identity in vitro and in vivo. Loss of Treg identity via genetic or transient BMI1 depletion perturbs the epigenome and converts Tregs into Th1/Th17-like proinflammatory cells, a transition relevant to human Crohn's disease associated CD4+ T cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.