ArticleThe Journal of experimental medicine2003
Normal incidence of diabetes in NOD mice tolerant to glutamic acid decarboxylase.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 86 citations in OpenAlex.
- Tipping the balance in autoimmunity: are regulatory t cells the cause, the cure, or both?Molecular and cellular pediatrics · 2024Review
- The beta cell-immune cell interface in type 1 diabetes (T1D).Molecular metabolism · 2023Review
- Monitoring immunomodulation strategies in type 1 diabetes.Frontiers in immunology · 2023Review
- Elevated histone H3 acetylation is associated with genes involved in T lymphocyte activation and glutamate decarboxylase antibody production in patients with type 1 diabetes.Journal of diabetes investigation · 2019Article
- APC-targeted proinsulin expression inactivates insulin-specific memory CD8Immunology and cell biology · 2017Article
- Understanding Autoimmune Diabetes through the Prism of the Tri-Molecular Complex.Frontiers in endocrinology · 2017Review
- Identification of Candidate Tolerogenic CD8(+) T Cell Epitopes for Therapy of Type 1 Diabetes in the NOD Mouse Model.Journal of diabetes research · 2016Article
- Oral Administration of Silkworm-Produced GAD65 and Insulin Bi-Autoantigens against Type 1 Diabetes.PloS one · 2016Article
- MAS-1 adjuvant immunotherapy generates robust Th2 type and regulatory immune responses providing long-term protection from diabetes in late-stage pre-diabetic NOD mice.Autoimmunity · 2014Article
- Monoclonal antibody blocking the recognition of an insulin peptide-MHC complex modulates type 1 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Trials in type 1 diabetes: Antigen-specific therapies.Clinical immunology (Orlando, Fla.) · 2013Review
- Antigen-based vaccination and prevention of type 1 diabetes.Current diabetes reports · 2013Review
- 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
- Antigen-specific therapeutic approaches in Type 1 diabetes.Cold Spring Harbor perspectives in medicine · 2012Review
- Pathogenic mechanisms in type 1 diabetes: the islet is both target and driver of disease.The review of diabetic studies : RDS · 2012Review
- Insulin as a key autoantigen in the development of type 1 diabetes.Diabetes/metabolism research and reviews · 2011Review
- Prevention of type 1 diabetes in mice by tolerogenic vaccination with a strong agonist insulin mimetope.The Journal of experimental medicine · 2011Article
- Suppression of dendritic cell activation by diabetes autoantigens linked to the cholera toxin B subunit.Immunobiology · 2011Article
- Antigen-based immune therapeutics for type 1 diabetes: magic bullets or ordinary blanks?Clinical & developmental immunology · 2011Article
- Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Experiments in nonobese diabetic (NOD) mice that lacked expression of glutamic acid decarboxylase (GAD) in beta cells have suggested that GAD represents an autoantigen essential for initiating and maintaining the diabetogenic immune response. Several attempts of inducing GAD-specific recessive tolerance to support this hypothesis have failed. Here we report on successful tolerance induction by expressing a modified form of GAD under control of the invariant chain promoter resulting in efficient epitope display. In spite of specific tolerance insulitis and diabetes occurred with normal kinetics indicating that GAD is not an essential autoantigen in the pathogenesis of diabetes.
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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.