ArticleThe Journal of experimental medicine1993
Glutamic acid decarboxylase 67-reactive T cells: a marker of insulin-dependent diabetes.
Article in The Journal of experimental medicine, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 110 citations in OpenAlex.
- Antigen Presentation, Autoantigens, and Immune Regulation in Multiple Sclerosis and Other Autoimmune Diseases.Frontiers in immunology · 2015Review
- Antigen-specific therapeutic approaches in Type 1 diabetes.Cold Spring Harbor perspectives in medicine · 2012Review
- T cell recognition of autoantigens in human type 1 diabetes: clinical perspectives.Clinical & developmental immunology · 2011Review
- An update on the use of NOD mice to study autoimmune (Type 1) diabetes.Expert review of clinical immunology · 2010Article
- T-cell epitopes in type 1 diabetes.Current diabetes reports · 2004Review
- Review
- T-cell reactivity to glutamic acid decarboxylase in stiff-man syndrome and cerebellar ataxia associated with polyendocrine autoimmunity.Clinical and experimental immunology · 2002Article
- Evidence for recognition of novel islet T cell antigens by granule-specific T cell lines from new onset type 1 diabetic patients.Clinical and experimental immunology · 2000Article
- Autoimmunity to glutamic acid decarboxylase in patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED).Clinical and experimental immunology · 2000Article
- Increased bcl-2 expression in lymphocytes and its association with hepatocellular damage in patients with autoimmune hepatitis.Clinical and experimental immunology · 1999Article
- Identification of naturally processed T cell epitopes from glutamic acid decarboxylase presented in the context of HLA-DR alleles by T lymphocytes of recent onset IDDM patients.The Journal of clinical investigation · 1997Article
- Common T cell receptor clonotype in lacrimal glands and labial salivary glands from patients with Sjögren's syndrome.The Journal of clinical investigation · 1996Article
- A role of Hsp60 in autoimmune diabetes: analysis in a transgenic model.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Antigen-specific therapy for autoimmune disease: prospects for the prevention of insulin-dependent diabetes.Molecular medicine (Cambridge, Mass.) · 1995Review
- Dual T cell receptor alpha chain T cells in autoimmunity.The Journal of experimental medicine · 1995Article
- Similar peptides from two beta cell autoantigens, proinsulin and glutamic acid decarboxylase, stimulate T cells of individuals at risk for insulin-dependent diabetes.Molecular medicine (Cambridge, Mass.) · 1995Article
- Experimental autoimmune insulitis. Induction by T lymphocytes specific for a peptide of proinsulin.The American journal of pathology · 1995Article
- HLA DRB4 0101-restricted immunodominant T cell autoepitope of pyruvate dehydrogenase complex in primary biliary cirrhosis: evidence of molecular mimicry in human autoimmune diseases.The Journal of experimental medicine · 1995Article
- Isolation by anion-exchange of immunologically and enzymatically active human islet glutamic acid decarboxylase 65 overexpressed in Sf9 insect cells.Diabetologia · 1995Article
- Cellular immunity to a determinant common to glutamate decarboxylase and coxsackie virus in insulin-dependent diabetes.The Journal of clinical investigation · 1994Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamic acid decarboxylase (GAD) has been shown to be a target of autoantibodies in insulin-dependent diabetes (IDD). Two forms of GAD, with molecular weights of 67,000 and 65,000, have been cloned from separate genes. As pancreatic islet beta cell destruction DD is an autoimmune process mediated by T cells, we sought to determine if recombinant GAD67 was recognized by T cells in IDD subjects and particularly their first-degree relatives with islet cell antibodies known to be at risk for IDD. The central regions of human islet and brain GAD67 (amino acids 208-404) were cloned as fusion proteins with glutathione-S-transferase (GST). Proliferation of peripheral blood T cells in the presence of recombinant GAD67 was significantly higher in both at-risk relatives and recent-onset IDD subjects than in other autoimmune disease subjects and human histocompatibility leukocyte antigen (HLA)-matched healthy controls. Thus, 12 of 29 (41%) at-risk relatives and 11 of 29 (38%) recent-onset IDD subjects responded to GAD67, compared with 1 of 7 (14%) other autoimmune disease subjects and 1 of 23 (4%) HLA-matched controls. T cell responses to GST alone or to tetanus toxoid were not different between the groups. These findings demonstrate that GAD67 is a target autoantigen of T cells in IDD and suggest the possibility that GAD-reactive T cells may delineate asymptomatic subjects at increased risk for IDD.
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