ArticleProceedings of the National Academy of Sciences of the United States of America2007
Adaptive TGF-beta-dependent regulatory T cells control autoimmune diabetes and are a privileged target of anti-CD3 antibody treatment.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
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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
79 citing papers in PubMed, 175 citations in OpenAlex.
- Trial
- Treatment of patients with new onset Type 1 diabetes with a single course of anti-CD3 mAb Teplizumab preserves insulin production for up to 5 years.Clinical immunology (Orlando, Fla.) · 2009Trial
- The effect of costimulatory and interleukin 2 receptor blockade on regulatory T cells in renal transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2008Trial
- Redosing of anti-CD3 antibodies in NOD mice with new-onset diabetes does not alter the effect of a single treatment course.Diabetologia · 2026Article
- Combination of proton-pump inhibitor and anti-CD3 F(ab')Immunotherapy advances · 2026Article
- Therapeutic Antibodies in Medicine.Molecules (Basel, Switzerland) · 2023Review
- Teplizumab: type 1 diabetes mellitus preventable?European journal of clinical pharmacology · 2023Review
- Regulatory T cell homeostasis: Requisite signals and implications for clinical development of biologics.Clinical immunology (Orlando, Fla.) · 2023Review
- Regulatory T cells in skeletal muscle repair and regeneration: recent insights.Cell death & disease · 2022Review
- The crucial role of early-life gut microbiota in the development of type 1 diabetes.Acta diabetologica · 2021Review
- 100 years post-insulin: immunotherapy as the next frontier in type 1 diabetes.Immunotherapy advances · 2021Review
- Immunological Impact of Intestinal T Cells on Metabolic Diseases.Frontiers in immunology · 2021Review
- Evolving Antibody Therapies for the Treatment of Type 1 Diabetes.Frontiers in immunology · 2020Review
- Evaluating the Causal Role of Gut Microbiota in Type 1 Diabetes and Its Possible Pathogenic Mechanisms.Frontiers in endocrinology · 2020Review
- Immunotherapy with oral administration of humanized anti-CD3 monoclonal antibody: a novel gut-immune system-based therapy for metaflammation and NASH.Clinical and experimental immunology · 2018Review
- Article
- The Proteasome Inhibitor Bortezomib Controls Indoleamine 2,3-Dioxygenase 1 Breakdown and Restores Immune Regulation in Autoimmune Diabetes.Frontiers in immunology · 2017Article
- Age-related Defects in Ocular and Nasal Mucosal Immune System and the Immunopathology of Dry Eye Disease.Ocular immunology and inflammation · 2016Review
- Regulatory T cells turn pathogenic.Cellular & molecular immunology · 2015Review
- T cell subsets and their signature cytokines in autoimmune and inflammatory diseases.Cytokine · 2015Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous results have shown that CD4(+)CD25(+) regulatory T cells (Tregs) control autoimmunity in a spontaneous model of type 1 diabetes, the nonobese diabetic (NOD) mouse. Moreover, anti-CD3 reverses diabetes in this setting by promoting Tregs that function in a TGF-beta-dependent manner. This finding contrasts with a large body of work suggesting that CD4(+)CD25(high) Tregs act in a cytokine-independent manner, thus suggesting that another type of Treg is operational in this setting. We sought to determine the basis of suppression both in untreated NOD mice and in those treated with anti-CD3. Our present results show that a subset of foxP3(+) cells present within a CD4(+)CD25(low) lymphocyte subset suppresses T cell immunity in spontaneously diabetic NOD mice in a TGF-beta-dependent manner, a functional property typical of "adaptive" regulatory T cells. This distinct Treg subset is evident in NOD, but not normal, mice, suggesting that the NOD mice may generate these adaptive Tregs in an attempt to regulate ongoing autoimmunity. Importantly, in two distinct in vivo models, these TGF-beta-dependent adaptive CD4(+)CD25(low) T cells can be induced from peripheral CD4(+)CD25(-) T lymphocytes by anti-CD3 immunotherapy which correlates with the restoration of self-tolerance.
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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.