ArticleThe Journal of clinical investigation1998
GAD-reactive CD4+ Th1 cells induce diabetes in NOD/SCID mice.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 154 citations in OpenAlex.
- Antigen-specific T cell responses in autoimmune diabetes.Frontiers in immunology · 2024Review
- HLA-DR3 mediated CD4 T cell response against GAD65 in type 1 diabetes patients.Journal of diabetes · 2023Article
- T-Cell Receptor/HLA Humanized Mice Reveal Reduced Tolerance and Increased Immunogenicity of Posttranslationally Modified GAD65 Epitope.Diabetes · 2022Article
- Noncontiguous T cell epitopes in autoimmune diabetes: From mice to men and back again.The Journal of biological chemistry · 2021Review
- GAD antibodies in neurological disorders - insights and challenges.Nature reviews. Neurology · 2020Review
- Understanding Autoimmune Diabetes through the Prism of the Tri-Molecular Complex.Frontiers in endocrinology · 2017Review
- Mechanisms of diabetic autoimmunity: I--the inductive interface between islets and the immune system at onset of inflammation.Immunologic research · 2016Review
- Mechanisms of diabetic autoimmunity: II--Is diabetes a central or peripheral disorder of effector and regulatory cells?Immunologic research · 2016Review
- IGRP and insulin vaccination induce CD8+ T cell-mediated autoimmune diabetes in the RIP-CD80GP mouse.Clinical and experimental immunology · 2014Article
- CD4+ T cells recognize diverse epitopes within GAD65: implications for repertoire development and diabetes monitoring.Immunology · 2013Article
- Novel autoantigens in type 1 diabetes.American journal of translational research · 2013Article
- Pathogenesis of NOD diabetes is initiated by reactivity to the insulin B chain 9-23 epitope and involves functional epitope spreading.Journal of autoimmunity · 2012Article
- Identification of new autoantigens by protein array indicates a role for IL4 neutralization in autoimmune hepatitis.Molecular & cellular proteomics : MCP · 2012Article
- Antigen-specific therapeutic approaches in Type 1 diabetes.Cold Spring Harbor perspectives in medicine · 2012Review
- Making the most of major histocompatibility complex molecule multimers: applications in type 1 diabetes.Clinical & developmental immunology · 2012Review
- B Cell in Autoimmune Diseases.Scientifica · 2012Article
- Anti-idiotypic antibody specific to GAD65 autoantibody prevents type 1 diabetes in the NOD mouse.PloS one · 2012Article
- IL-13Rα1 expression on β-cell-specific T cells in NOD mice.Diabetes · 2011Article
- T cell recognition of autoantigens in human type 1 diabetes: clinical perspectives.Clinical & developmental immunology · 2011Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Although glutamic acid decarboxylase (GAD) has been implicated in IDDM, there is no direct evidence showing GAD-reactive T cells are diabetogenic in vivo. To address this issue, 3-wk-old NOD mice received two injections of purified rat brain GAD; one mouse rapidly developed diabetes 3 wk later. Splenocytes from this mouse showed a proliferative response to purified GAD, and were used to generate a CD4+ T cell line, designated 5A, that expresses TCRs encoding Vbeta2 and Vbeta12. 5A T cells exhibit a MHC restricted proliferative response to purified GAD, as well as GAD65 peptide 524-543. After antigen-specific stimulation, 5A T cells secrete IFNgamma and TNFalpha/beta, but not IL-4. They are also cytotoxic against NOD-derived hybridoma cells (expressing I-Ag7) that were transfected with rat GAD65, but not nontransfected hybridoma cells. Adoptive transfer of 5A cells into NOD/SCID mice produced insulitis in all mice. Diabetes occurred in 83% of the mice. We conclude that GAD injection in young NOD mice may, in some cases, provoke diabetes due to the activation of diabetogenic T cells reactive to GAD65 peptides. Our data provide direct evidence that GAD65 autoimmunity may be a critical event in the pathogenesis of IDDM.
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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.