ArticleNature immunology2014
The epigenetic regulator Uhrf1 facilitates the proliferation and maturation of colonic regulatory T cells.
Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
103 citing papers in PubMed, 182 citations in OpenAlex.
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- Epigenetic Alterations in Microbiome-Host Interactions in Inflammatory and Autoimmune Diseases.International journal of molecular sciences · 2026Review
- UHRF1 deficiency exacerbates intestinal inflammation by epigenetic modulation of NPY1R gene methylation.JCI insight · 2026Article
- The roles of cell cycle proteins in regulating the tumor immune microenvironment.Genes & diseases · 2026Review
- Fetal programming by the parental microbiome of offspring behavior, and DNA methylation and gene expression within the hippocampus.Microbiome · 2025Article
- Gut microbiota and epigenetic inheritance: implications for the development of IBD.Gut microbes · 2025Review
- A Hybrid compound H93 treats prostate cancer by directly binding UHRF1 and promoting protein dimerization.Communications chemistry · 2025Article
- UHRF1 in endothelial cells is essential for angiogenesis and associated with the activation of pro-angiogenic signaling pathways and expression of endothelial genes.Angiogenesis · 2025Article
- UHRF1 in Immune Regulation and Diseases: Mechanisms and Therapeutic Implications.Clinical reviews in allergy & immunology · 2025Review
- Epigenetic modifications of gut microbiota and their potential role in atherosclerosis.Frontiers in pharmacology · 2025Review
- CDK4/6 inhibitors in breast cancer therapy: mechanisms of drug resistance and strategies for treatment.Frontiers in pharmacology · 2025Review
- Directed disruption of IL2 aggregation and receptor binding sites produces designer biologics with enhanced specificity and improved production capacity.Computational and structural biotechnology journal · 2025Article
- Hyperactivating EZH2 to augment H3K27me3 levels in regulatory T cells enhances immune suppression by driving early effector differentiation.Cell reports · 2024Article
- Strategies for targeting cytokines in inflammatory bowel disease.Nature reviews. Immunology · 2024Review
- Dual Regulation Mechanism of Obesity: DNA Methylation and Intestinal Flora.Biomedicines · 2024Review
- Beneficial Effects of Dietary Fiber in Young Barley Leaf on Gut Microbiota and Immunity in Mice.Molecules (Basel, Switzerland) · 2024Article
- Non-Mutational Key Features in the Biology of Thymomas.Cancers · 2024Review
- Targeting G9a/DNMT1 methyltransferase activity impedes IGF2-mediated survival in hepatoblastoma.Hepatology communications · 2024Article
- Deciphering the developmental trajectory of tissue-resident Foxp3Frontiers in immunology · 2024Review
43 more citing papers are in PubMed but not listed here.
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Authors and funding
22 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal regulatory T cells (Treg cells) are necessary for the suppression of excessive immune responses to commensal bacteria. However, the molecular machinery that controls the homeostasis of intestinal Treg cells has remained largely unknown. Here we report that colonization of germ-free mice with gut microbiota upregulated expression of the DNA-methylation adaptor Uhrf1 in Treg cells. Mice with T cell-specific deficiency in Uhrf1 (Uhrf1(fl/fl)Cd4-Cre mice) showed defective proliferation and functional maturation of colonic Treg cells. Uhrf1 deficiency resulted in derepression of the gene (Cdkn1a) that encodes the cyclin-dependent kinase inhibitor p21 due to hypomethylation of its promoter region, which resulted in cell-cycle arrest of Treg cells. As a consequence, Uhrf1(fl/fl)Cd4-Cre mice spontaneously developed severe colitis. Thus, Uhrf1-dependent epigenetic silencing of Cdkn1a was required for the maintenance of gut immunological homeostasis. This mechanism enforces symbiotic host-microbe interactions without an inflammatory response.
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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.