ArticleDiabetes2012
Following the fate of one insulin-reactive CD4 T cell: conversion into Teffs and Tregs in the periphery controls diabetes in NOD mice.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Discovery of Glucose Metabolism-Associated Genes in Neuropathic Pain: Insights from Bioinformatics.International journal of molecular sciences · 2024Article
- Immunological and virological triggers of type 1 diabetes: insights and implications.Frontiers in immunology · 2023Review
- Intestinal Microbiota in Common Chronic Inflammatory Disorders Affecting Children.Frontiers in immunology · 2021Review
- Review
- Type 1 diabetes pathogenesis and the role of inhibitory receptors in islet tolerance.Annals of the New York Academy of Sciences · 2020Review
- MHC-mismatched mixed chimerism restores peripheral tolerance of noncross-reactive autoreactive T cells in NOD mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Protein Tyrosine Phosphatases: Regulators of CD4 T Cells in Inflammatory Bowel Disease.Frontiers in immunology · 2018Review
- Cutting Edge: Dual TCRα Expression Poses an Autoimmune Hazard by Limiting Regulatory T Cell Generation.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Beta-cell Specific Autoantibodies: Are they Just an Indicator of Type 1 Diabetes?Current diabetes reviews · 2017Review
- Restoring Regulatory T Cells in Type 1 Diabetes.Current diabetes reports · 2016Review
- The protein tyrosine phosphatase PTPN22 controls forkhead box protein 3 T regulatory cell induction but is dispensable for T helper type 1 cell polarization.Clinical and experimental immunology · 2014Article
- TCR affinity and tolerance mechanisms converge to shape T cell diabetogenic potential.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Lymphopenia-induced proliferation in aire-deficient mice helps to explain their autoimmunity and differences from human patients.Frontiers in immunology · 2014Review
- Article
- Chronic follicular bronchiolitis requires antigen-specific regulatory T cell control to prevent fatal disease progression.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Pathogenic CD4⁺ T cells recognizing an unstable peptide of insulin are directly recruited into islets bypassing local lymph nodes.The Journal of experimental medicine · 2013Article
- Advances in distinguishing natural from induced Foxp3(+) regulatory T cells.International journal of clinical and experimental pathology · 2013Review
- Neuropilin-1 distinguishes natural and inducible regulatory T cells among regulatory T cell subsets in vivo.The Journal of experimental medicine · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
In diabetic patients and susceptible mice, insulin is a targeted autoantigen. Insulin B chain 9-23 (B:9-23) autoreactive CD4 T cells are key for initiating autoimmune diabetes in NOD mice; however, little is known regarding their origin and function. To this end, B:9-23-specific, BDC12-4.1 T-cell receptor (TCR) transgenic (Tg) mice were studied, of which, despite expressing a single TCR on the recombination activating gene-deficient background, only a fraction develops diabetes in an asynchronous manner. BDC12-4.1 CD4 T cells convert into effector (Teff) and Foxp3(+)-expressing adaptive regulatory T cells (aTregs) soon after leaving the thymus as a result of antigen recognition and homeostatic proliferation. The generation of aTreg causes the heterogeneous diabetes onset, since crossing onto the scurfy (Foxp3) mutation, BDC12-4.1 TCR Tg mice develop accelerated and fully penetrant diabetes. Similarly, adoptive transfer and bone marrow transplantation experiments showed differential diabetes kinetics based on Foxp3(+) aTreg's presence in the BDC12-4.1 donors. A single-specificity, insulin-reactive TCR escapes thymic deletion and simultaneously converts into aTreg and Teff, establishing an equilibrium that determines diabetes penetrance. These results are of particular importance for understanding disease pathogenesis. They suggest that once central tolerance is bypassed, autoreactive cells arriving in the periphery do not by default follow solely a pathogenic fate upon activation.
Indexed as
Identifiers
What OpenQuestion holds
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.