ArticleThe Journal of clinical investigation2006
TGF-beta signaling is required for the function of insulin-reactive T regulatory cells.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 47 citations in OpenAlex.
- Bone Morphogenetic Proteins Shape TFrontiers in immunology · 2022Review
- Insulin-Reactive T Cells Convert Diabetogenic Insulin-Reactive VH125 B Cells Into Tolerogenic Cells by Reducing Germinal Center T:B Cell Interactions in NOD Mice.Frontiers in immunology · 2020Article
- A Novel Liposome Formulation Carrying Both an Insulin Peptide and a Ligand for Invariant Natural Killer T Cells Induces Accumulation of Regulatory T Cells to Islets in Nonobese Diabetic Mice.Journal of diabetes research · 2019Article
- Understanding Autoimmune Diabetes through the Prism of the Tri-Molecular Complex.Frontiers in endocrinology · 2017Review
- Immunoregulation by members of the TGFβ superfamily.Nature reviews. Immunology · 2016Review
- Altered connexin 43 expression underlies age-dependent decrease of regulatory T cell suppressor function in nonobese diabetic mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Article
- 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
- Following the fate of one insulin-reactive CD4 T cell: conversion into Teffs and Tregs in the periphery controls diabetes in NOD mice.Diabetes · 2012Article
- Germline TRAV5D-4 T-cell receptor sequence targets a primary insulin peptide of NOD mice.Diabetes · 2012Article
- Banting Lecture 2009: An unfinished journey: molecular pathogenesis to prevention of type 1A diabetes.Diabetes · 2010Article
- Analysis of T cell receptor beta chains that combine with dominant conserved TRAV5D-4*04 anti-insulin B:9-23 alpha chains.Journal of autoimmunity · 2009Article
- Regulatory T cells enter the pancreas during suppression of type 1 diabetes and inhibit effector T cells and macrophages in a TGF-beta-dependent manner.European journal of immunology · 2009Article
- Conserved T cell receptor alpha-chain induces insulin autoantibodies.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Insulin as an autoantigen in NOD/human diabetes.Current opinion in immunology · 2008Review
- Treatment with CD20-specific antibody prevents and reverses autoimmune diabetes in mice.The Journal of clinical investigation · 2007Article
- Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity.The Journal of clinical investigation · 2007Article
- Diabetes in non-obese diabetic mice is not associated with quantitative changes in CD4+ CD25+ Foxp3+ regulatory T cells.Immunology · 2007Article
- Translational mini-review series on type 1 diabetes: Systematic analysis of T cell epitopes in autoimmune diabetes.Clinical and experimental immunology · 2007Review
- An immunologic homunculus for type 1 diabetes.The Journal of clinical investigation · 2006Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
We have previously isolated insulin-reactive Tregs from diabetic NOD mice designated 2H6, from which TCR transgenic mice were generated. The T cells from these 2H6 transgenic mice recognize insulin but have suppressive properties in vitro. They protect NOD mice in vivo from spontaneous development of diabetes and adoptive transfer of disease caused by polyclonal diabetogenic spleen cells as well as the highly diabetogenic monoclonal BDC2.5 TCR transgenic T cells that recognize an islet granule antigen. Using cells from both NOD and BDC2.5 mice that express a dominant-negative TGF-beta receptor type II (TGF-betaDNRII), we show that 2H6 T cells protected from disease by producing TGF-beta and that the ability of the target diabetogenic T cells to respond to TGF-beta was crucial. We further demonstrate that TGF-beta signaling in 2H6 cells was important for their protective properties, as 2H6 cells were unable to protect from adoptive transfer-induced diabetes if they were unable to respond to TGF-beta. Thus, our data demonstrate that insulin-specific regulatory cells protect from diabetes by virtue of their production of TGF-beta1 that acts in an autocrine manner to maintain their regulatory function and acts in a paracrine manner on the target cells.
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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.