ArticleThe Journal of experimental medicine2002
CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 83 citations in OpenAlex.
- HLA-DR3 mediated CD4 T cell response against GAD65 in type 1 diabetes patients.Journal of diabetes · 2023Article
- Characterization of Peripheral Blood TCR in Patients with Type 1 Diabetes Mellitus by BD RhapsodyCells · 2022Article
- T-Cell Receptor/HLA Humanized Mice Reveal Reduced Tolerance and Increased Immunogenicity of Posttranslationally Modified GAD65 Epitope.Diabetes · 2022Article
- Antigen-Specific T Cell Analysis Reveals That Active Immune Responses to β Cell Antigens Are Focused on a Unique Set of Epitopes.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Efficient Presentation of Multiple Endogenous Epitopes to Both CD4Molecular therapy. Methods & clinical development · 2017Article
- CD52 as both a marker and an effector molecule of T cells with regulatory action: Identification of novel regulatory T cells.Cellular & molecular immunology · 2013Article
- Review
- Article
- Glutamic acid decarboxylase-derived epitopes with specific domains expand CD4(+)CD25(+) regulatory T cells.PloS one · 2009Article
- Recombinase-activating gene 1-associated expression of the myelin basic protein 1-11-specific transgenic T-cell receptor in H-2b mice.Journal of neuroscience research · 2009Article
- T-cell promiscuity in autoimmune diabetes.Diabetes · 2008Article
- Autoreactive human T-cell receptor initiates insulitis and impaired glucose tolerance in HLA DR4 transgenic mice.Journal of autoimmunity · 2008Article
- Parameters influencing antigen-specific immunotherapy for type 1 diabetes.Immunologic research · 2008Article
- Parameters influencing antigen-specific immunotherapy for Type 1 diabetes.Immunologic research · 2008Article
- Translational mini-review series on type 1 diabetes: Systematic analysis of T cell epitopes in autoimmune diabetes.Clinical and experimental immunology · 2007Review
- Age-dependent loss of tolerance to an immunodominant epitope of glutamic acid decarboxylase in diabetic-prone RIP-B7/DR4 mice.Clinical immunology (Orlando, Fla.) · 2006Article
- TGF-beta signaling is required for the function of insulin-reactive T regulatory cells.The Journal of clinical investigation · 2006Article
- Regulatory T cells and type 1 diabetes.Current diabetes reports · 2005Review
- Specific antigen vaccination to treat autoimmune disease.Proceedings of the National Academy of Sciences of the United States of America · 2004Review
- N-acetyl-cysteine accelerates transfer of diabetes into non-obese diabetic scid mice.Diabetologia · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Glutamic acid decarboxylase (GAD)65 is an early and important antigen in both human diabetes mellitus and the nonobese diabetic (NOD) mouse. However, the exact role of GAD65-specific T cells in diabetes pathogenesis is unclear. T cell responses to GAD65 occur early in diabetes pathogenesis, yet only one GAD65-specific T cell clone of many identified can transfer diabetes. We have generated transgenic mice on the NOD background expressing a T cell receptor (TCR)-specific for peptide epitope 286-300 (p286) of GAD65. These mice have GAD65-specific CD4(+) T cells, as shown by staining with an I-A(g7)(p286) tetramer reagent. Lymphocytes from these TCR transgenic mice proliferate and make interferon gamma, interleukin (IL)-2, tumor necrosis factor (TNF)-alpha, and IL-10 when stimulated in vitro with GAD65 peptide 286-300, yet these TCR transgenic animals do not spontaneously develop diabetes, and insulitis is virtually undetectable. Furthermore, in vitro activated CD4 T cells from GAD 286 TCR transgenic mice express higher levels of CTL-associated antigen (CTLA)-4 than nontransgenic littermates. CD4(+) T cells, or p286-tetramer(+)CD4(+) Tcells, from GAD65 286-300-specific TCR transgenic mice delay diabetes induced in NOD.scid mice by diabetic NOD spleen cells. This data suggests that GAD65 peptide 286-300-specific T cells have disease protective capacity and are not pathogenic.
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.