ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Altered connexin 43 expression underlies age-dependent decrease of regulatory T cell suppressor function in nonobese diabetic mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Soil-derived microbiota induces T regulatory cells and protect against mouse colitis, metabolic disease, and sepsis.Gut microbes · 2026Article
- Regulatory T Cells in Diabetic Wound Healing: A Comprehensive Review.Journal of inflammation research · 2026Review
- Metabolism in the tumor microenvironment: implications for pathogenesis and therapeutics.Frontiers in immunology · 2025Review
- FANCD2 as a ferroptosis-related target for recurrent implantation failure by integrated bioinformatics and Mendelian randomization analysis.Journal of cellular and molecular medicine · 2024Article
- Bioinformatics Analysis Identifies Key Genes in Recurrent Implantation Failure Based on Immune Infiltration.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Self and microbiota-derived epitopes induce CD4Mucosal immunology · 2021Article
- Connexin-Mediated Signaling at the Immunological Synapse.International journal of molecular sciences · 2020Review
- T Regulatory Cells From Non-obese Diabetic Mice Show Low Responsiveness to IL-2 Stimulation and Exhibit Differential Expression of Anergy-Related and Ubiquitination Factors.Frontiers in immunology · 2019Article
- Tregs: Where We Are and What Comes Next?Frontiers in immunology · 2017Review
- Mind the Gaps in Tumor Immunity: Impact of Connexin-Mediated Intercellular Connections.Frontiers in immunology · 2017Review
- Cyclic AMP Represents a Crucial Component of Treg Cell-Mediated Immune Regulation.Frontiers in immunology · 2016Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Type 1 diabetes is one of the most extensively studied autoimmune diseases, but the cellular and molecular mechanisms leading to T cell-mediated destruction of insulin-producing β cells are still not well understood. In this study, we show that regulatory T cells (T(regs)) in NOD mice undergo age-dependent loss of suppressor functions exacerbated by the decreased ability of activated effector T cells to upregulate Foxp3 and generate T(regs) in the peripheral organs. This age-dependent loss is associated with reduced intercellular communication mediated by gap junctions, which is caused by impaired upregulation and decreased expression of connexin 43. Regulatory functions can be corrected, even in T cells isolated from aged, diabetic mice, by a synergistic activity of retinoic acid, TGF-β, and IL-2, which enhance connexin 43 and Foxp3 expression in T(regs) and restore the ability of conventional CD4(+) T cells to upregulate Foxp3 and generate peripherally derived T(regs). Moreover, we demonstrate that suppression mediated by T(regs) from diabetic mice is enhanced by a novel reagent, which facilitates gap junction aggregation. In summary, our report identifies gap junction-mediated intercellular communication as an important component of the T(reg) suppression mechanism compromised in NOD mice and suggests how T(reg) mediated immune regulation can be improved.
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