ArticleProceedings of the National Academy of Sciences of the United States of America2004
Prevention of type I diabetes transfer by glutamic acid decarboxylase 65 peptide 206-220-specific T cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 32 citations in OpenAlex.
- The role of islet autoantigen-specific T cells in the onset and treatment of type 1 diabetes mellitus.Frontiers in immunology · 2024Review
- HLA-DR3 mediated CD4 T cell response against GAD65 in type 1 diabetes patients.Journal of diabetes · 2023Article
- Peripheral blood mononuclear cells reactivity in recent-onset type I diabetes patients is directed against the leader peptide of preproinsulin, GAD65Frontiers in immunology · 2023Article
- T-Cell Receptor/HLA Humanized Mice Reveal Reduced Tolerance and Increased Immunogenicity of Posttranslationally Modified GAD65 Epitope.Diabetes · 2022Article
- Conjugates of Cell Adhesion Peptides for Therapeutics and Diagnostics Against Cancer and Autoimmune Diseases.Current topics in medicinal chemistry · 2017Review
- Article
- Banting Lecture 2009: An unfinished journey: molecular pathogenesis to prevention of type 1A diabetes.Diabetes · 2010Article
- Article
- Autoreactive human T-cell receptor initiates insulitis and impaired glucose tolerance in HLA DR4 transgenic mice.Journal of autoimmunity · 2008Article
- Innocuous IFNgamma induced by adjuvant-free antigen restores normoglycemia in NOD mice through inhibition of IL-17 production.The Journal of experimental medicine · 2008Article
- Translational mini-review series on type 1 diabetes: Systematic analysis of T cell epitopes in autoimmune diabetes.Clinical and experimental immunology · 2007Review
- Reovirus delays diabetes onset but does not prevent insulitis in nonobese diabetic mice.Journal of virology · 2006Article
- Regulatory T cells and type 1 diabetes.Current diabetes reports · 2005Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Glutamic acid decarboxylase (GAD) 65 is one of the major pancreatic antigens targeted by self-reactive T cells in type I diabetes mellitus. T cells specific for GAD65 are among the first to enter inflamed islets and may be important for the initiation of autoimmune diabetes. However, we previously reported that nonobese diabetic (NOD) mice transgenic for a T cell antigen receptor (TCR) specific for one of the immunodominant epitopes of GAD65, peptide 286-300 (G286), are protected from insulitis and diabetes. To examine whether other GAD65-reactive T cells share this phenotype, we have generated TCR transgenic NOD mice for a second immunodominant epitope of GAD65, peptide 206-220 (G206). As in G286 mice, G206 mice do not develop islet inflammation or diabetes. When adoptively transferred along with diabetogenic T cells, activated G206 T cells significantly delayed the onset of diabetes in NOD.scid recipients. Both G206 and G286 T cells produce immunoregulatory cytokines IFN-gamma and IL-10 at low levels when activated by cognate antigens. These data suggest that GAD65-specific T cells may play a protective role in diabetes pathogenesis by regulating pathogenic T cell responses. A better understanding of the functions of autoreactive T cells in type I diabetes will be necessary for choosing desirable targets for immunotherapy.
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