ArticleMolecular medicine (Cambridge, Mass.)2014
Low-dose 5-aza-2'-deoxycytidine pretreatment inhibits experimental autoimmune encephalomyelitis by induction of regulatory T cells.
Article in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Immune responses to azacytidine in animal models of inflammatory disorders: a systematic review.Journal of translational medicine · 2021Pooled it
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- Advances in Therapeutics Research for Demyelinating Diseases.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Neurotrophic factors in multiple sclerosis.Frontiers in immunology · 2025Review
- Epigenetic modification of CD4Cell death & disease · 2024Article
- The astrocyte-produced growth factor HB-EGF limits autoimmune CNS pathology.Nature immunology · 2024Article
- Autoimmune disease: a view of epigenetics and therapeutic targeting.Frontiers in immunology · 2024Review
- Multiple Sclerosis: New Insights into Molecular Pathogenesis and Novel Platforms for Disease Treatment.Current drug research reviews · 2024Review
- Differential roles of regulatory T cells in acute respiratory infections.The Journal of clinical investigation · 2023Review
- Global DNA Methylation and Hydroxymethylation Levels in PBMCs Are Altered in RRMS Patients Treated with IFN-β and GA-A Preliminary Study.International journal of molecular sciences · 2023Article
- Augmenting chemotherapy with low-dose decitabine through an immune-independent mechanism.JCI insight · 2022Article
- Epigenetic regulation of B cells and its role in autoimmune pathogenesis.Cellular & molecular immunology · 2022Review
- Epigenetic Control of Regulatory T Cell Stability and Function: Implications for Translation.Frontiers in immunology · 2022Review
- Non-Coding RNA in Systemic Sclerosis: A Valuable Tool for Translational and Personalized Medicine.Genes · 2021Review
- Regulatory T Cells-Related Genes Are under DNA Methylation Influence.International journal of molecular sciences · 2021Review
- m6A RNA Methylation in Systemic Autoimmune Diseases-A New Target for Epigenetic-Based Therapy?Pharmaceuticals (Basel, Switzerland) · 2021Review
- Metabolic Controls on Epigenetic Reprogramming in Regulatory T Cells.Frontiers in immunology · 2021Review
- Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function.The Journal of clinical investigation · 2020Article
- Pathogenic Roles of Autoantibodies and Aberrant Epigenetic Regulation of Immune and Connective Tissue Cells in the Tissue Fibrosis of Patients with Systemic Sclerosis.International journal of molecular sciences · 2020Review
- Low-Dose Decitabine Assists Human Umbilical Cord-Derived Mesenchymal Stem Cells in ProtectingStem cells international · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Forkhead box P3 (Foxp3) is the major transcription factor controlling the development and function of regulatory T (Treg) cells. Previous studies have indicated epigenetic regulation of Foxp3 expression. Here, we investigated whether the deoxyribonucleic acid (DNA) methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-Aza) applied peripherally could modulate central nervous system (CNS) inflammation, by using a mouse experimental autoimmune encephalomyelitis (EAE) model. We found that disease activity was inhibited in a myelin oligodendrocyte glycoprotein (MOG) peptide-induced EAE mouse briefly pretreated with low-dose (0.15 mg/kg) 5-Aza, ameliorating significant CNS inflammatory responses, as indicated by greatly decreased proinflammatory cytokines. On the contrary, control EAE mice expressed high levels of IFN-γ and interleukin (IL)-17. In addition, 5-Aza treatment in vitro increased GFP expression in CD4(+)GFP(-) T cells isolated from GFP knock-in Foxp3 transgenic mice. Importantly, 5-Aza treatment increased Treg cell numbers, in EAE mice, at both disease onset and peak. However, Treg inhibition assays showed 5-Aza treatment did not enhance per-cell Treg inhibitory function, but did maintain a lower activation threshold for effector cells in EAE mice. In conclusion, 5-Aza treatment prevented EAE development and suppressed CNS inflammation, by increasing the number of Treg cells and inhibiting effector cells in the periphery.
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