ArticleProceedings of the National Academy of Sciences of the United States of America2017
Intestinal type 1 regulatory T cells migrate to periphery to suppress diabetogenic T cells and prevent diabetes development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- The Commensal Microbiota and Viral Infection: A Comprehensive Review.Frontiers in immunology · 2019Pooled it
- Trial
- Trial
- The Role of Microbiota in Type 1 Diabetes: Insights into Dysbiosis and Immune Interactions.Nutrients · 2026Review
- Antigen-specific immunotherapy with a CD4Nature communications · 2026Article
- Multiple low dose streptozotocin-induced diabetes as a model for studying autoimmune diabetes in humans.Animal models and experimental medicine · 2025Review
- Microbiota-dependent modulation of intestinal anti-inflammatory CD4Seminars in immunopathology · 2025Review
- Review
- Mechanism of Action of OralVaccines · 2024Article
- Journey of Teplizumab: A Promising Drug in the Treatment of Type 1 Diabetes Mellitus.Current diabetes reviews · 2024Review
- Mechanistic Insights into Immune-Microbiota Interactions and Preventive Role of Probiotics Against Autoimmune Diabetes Mellitus.Probiotics and antimicrobial proteins · 2023Review
- Intestinal Tr1 Cells Confer Protection against Colitis in the Absence of Foxp3+ Regulatory T Cell-Derived IL-10.ImmunoHorizons · 2023Article
- Development of Type 1 Diabetes in Mice Is Associated with a Decrease in IL-2-Producing ILC3 and FoxP3Molecules (Basel, Switzerland) · 2023Article
- Type I regulatory T cells in malaria: of mice and men.The Journal of clinical investigation · 2023Article
- Virus induced dysbiosis promotes type 1 diabetes onset.Frontiers in immunology · 2023Article
- Highly purified and functionally stableFrontiers in immunology · 2023Article
- Combinations of anti-GITR antibody and CD28 superagonist induce permanent allograft acceptance by generating type 1 regulatory T cells.Science advances · 2022Article
- Increased levels of pathogenic Th17 cells and diminished function of CD69+ Treg lymphocytes in patients with overweight.Clinical and experimental immunology · 2022Article
- Elevated testicular apoptosis is associated with elevated sphingosine driven by gut microbiota in prediabetic sheep.BMC biology · 2022Article
- Activation pathways that drive CD4Immunological reviews · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Growing insight into the pathogenesis of autoimmune diseases and numerous studies in preclinical models highlights the potential of regulatory T cells to restore tolerance. By using non-obese diabetic (NOD) BDC2.5 TCR-transgenic (Tg), and IL-10 and Foxp3 double-reporter mice, we demonstrate that alteration of gut microbiota during cohousing experiments or treatment with anti-CD3 mAb significantly increase intestinal IL-10-producing type 1 regulatory T (Tr1) cells and decrease diabetes incidence. These intestinal antigen-specific Tr1 cells have the ability to migrate to the periphery via a variety of chemokine receptors such as CCR4, CCR5, and CCR7 and to suppress proliferation of Th1 cells in the pancreas. The ability of Tr1 cells to cure diabetes in NOD mice required IL-10 signaling, as Tr1 cells could not suppress CD4
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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.