ArticleJournal of molecular medicine (Berlin, Germany)2009
Induction of Foxp3 demethylation increases regulatory CD4+CD25+ T cells and prevents the occurrence of diabetes in mice.
Article in Journal of molecular medicine (Berlin, Germany), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Immune responses to azacytidine in animal models of inflammatory disorders: a systematic review.Journal of translational medicine · 2021Pooled it
- An Update Comprehensive Review on Epigenetic Modifications and Therapies in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2026Review
- Review
- Ten-Eleven Translocation Family Proteins: Structure, Biological Functions, Diseases, and Targeted Therapy.MedComm · 2025Review
- Hypomethylating therapy mitigates acute allograft rejection in a murine lung transplant model.Frontiers in transplantation · 2025Article
- Exploring the key role of DNA methylation as an epigenetic modulator in oxidative stress related islet cell injury in patients with type 2 diabetes mellitus: a review.Journal of diabetes and metabolic disorders · 2024Review
- Immunomodulation for Tissue Repair and Regeneration.Tissue engineering and regenerative medicine · 2023Review
- Augmenting chemotherapy with low-dose decitabine through an immune-independent mechanism.JCI insight · 2022Article
- Oxidative stress-mediated beta cell death and dysfunction as a target for diabetes management.Frontiers in endocrinology · 2022Review
- Nature vs. nurture: FOXP3, genetics, and tissue environment shape Treg function.Frontiers in immunology · 2022Review
- Low-dose decitabine modulates T-cell homeostasis and restores immune tolerance in immune thrombocytopenia.Blood · 2021Article
- Epigenetic DNA Methylation ofInternational journal of molecular sciences · 2021Article
- Prostaglandin E2 Reverses the Effects of DNA Methyltransferase Inhibitor and TGFB1 on the Conversion of Naive T Cells to iTregs.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2020Article
- Autoimmune thyroid disease and type 1 diabetes mellitus: same pathogenesis; new perspective?Therapeutic advances in endocrinology and metabolism · 2020Review
- Effects of Treatment with the Hypomethylating Agent 5-aza-2'-deoxycytidine in Murine Type II Collagen-Induced Arthritis.Pharmaceuticals (Basel, Switzerland) · 2019Article
- The DNA Methylation Inhibitor Zebularine Controls CD4Frontiers in immunology · 2019Article
- Environmental Factors Associated With Type 1 Diabetes.Frontiers in endocrinology · 2019Review
- Epigenetic regulation in B-cell maturation and its dysregulation in autoimmunity.Cellular & molecular immunology · 2018Review
- DNA Methyltransferase Inhibition Promotes Th1 Polarization in Human CD4Journal of immunology research · 2018Article
- The Role of Histone Methyltransferases and Long Non-coding RNAs in the Regulation of T Cell Fate Decisions.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD4(+)CD25(+) regulatory T cells (Treg), a subpopulation of CD4(+) T cells, regulate immune responses. Foxp3 is a key transcription factor for the development and function of Treg cells. During T-cell activation in vitro, a DNA demethylation agent 5-Aza-2'-deoxycytydine (DAC) can induce Foxp3 expression in CD4(+)CD25(-) Foxp3(-) cells via altering methylation status of a conserved element in the 5'-untranslated region of the Foxp3 gene. However, the effects of this agent on the development of Foxp3(+) Treg cells in the thymus and in vivo are poorly understood. In the present study, a short-term treatment with a low dose of DAC significantly increased the ratios of thymic CD4(+)CD8(-) CD25(+) cells or CD4(+)CD8(-) Foxp3(+) cells to CD4(+)CD8(-) cells, and the total numbers of thymic CD4(+)CD8(-)Foxp3(+) Treg cells or CD4(+)CD8(-)CD25(+)Foxp3(+) Treg cells in the thymus in mice. DAC-treatment induced the Foxp3 expression and the significant demethylation of a CpG island in the first intron of the Foxp3 gene in CD4(+)CD8(-)CD25(+) cells predominantly. Furthermore, CD4(+)CD8(-)CD25(+) thymocytes in DAC-treated mice exhibited enhanced immunosuppressive function than those in control mice. In addition, DAC treatment in vivo was effective in improving the clinical course of diabetes in cyclophosphamide (CY)-potentiated non-obese diabetic mice (CY-NOD). Thus, the in vivo treatment with DAC can significantly promote the development of natural thymic CD4(+)CD25(+)Foxp3(+) Treg cells through Foxp3 demethylation, implicating a therapeutic application of DAC in patients suffering from autoimmune diseases.
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