ArticleProceedings of the National Academy of Sciences of the United States of America1992
Glutamic acid decarboxylase autoantibodies in preclinical insulin-dependent diabetes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. 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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13 citing papers in PubMed, 57 citations in OpenAlex.
- Methylation-induced suppression of BEX1 activates AKT/ERK/STAT3 signaling pathways regulating cell cycle and apoptosis in glioma.Scientific reports · 2025Article
- Trials in type 1 diabetes: Antigen-specific therapies.Clinical immunology (Orlando, Fla.) · 2013Review
- Antigen-specific therapeutic approaches in Type 1 diabetes.Cold Spring Harbor perspectives in medicine · 2012Review
- Clinical potential of antigen-specific therapies in type 1 diabetes.The review of diabetic studies : RDS · 2012Review
- Transplantation of GABA-producing cells for seizure control in models of temporal lobe epilepsy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009Review
- GABAergic neurons in barrel cortex show strong, whisker-dependent metabolic activation during normal behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
- IA-2, a transmembrane protein of the protein tyrosine phosphatase family, is a major autoantigen in insulin-dependent diabetes mellitus.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
- A protective role of gamma delta T cells in primary infection with Listeria monocytogenes in autoimmune non-obese diabetic mice.Immunology · 1995Article
- Isolation by anion-exchange of immunologically and enzymatically active human islet glutamic acid decarboxylase 65 overexpressed in Sf9 insect cells.Diabetologia · 1995Article
- Anti-glutamate decarboxylase and other antibodies at the onset of childhood IDDM: a population-based study.Diabetologia · 1994Article
- Prevalence of autoantibodies to the 65- and 67-kD isoforms of glutamate decarboxylase in insulin-dependent diabetes mellitus.The Journal of clinical investigation · 1993Article
- Glutamic acid decarboxylase 67-reactive T cells: a marker of insulin-dependent diabetes.The Journal of experimental medicine · 1993Article
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
Insulin-dependent diabetes mellitus (IDDM) is associated with serum antibodies that precipitate a 64-kDa pancreatic islet cell protein reported to be glutamic acid decarboxylase (GAD; glutamate decarboxylase, EC 4.1.1.15). Previously, antibodies to GAD were found in the rare neurological disorder stiff man syndrome. To demonstrate directly antibodies to GAD, enzymatically active GAD was first purified from fresh human cerebellum. Brain GAD activity was precipitated by noninhibitory antibodies in the sera of 16/26 (62%) subjects defined as having preclinical IDDM (islet cell antibody-positive first-degree relatives of a person with IDDM), 3/13 (23%) with recent-onset IDDM, and 3/3 with the stiff man syndrome. In addition, sera of 5/26 (19%) preclinical and 2/13 (15%) recent-onset IDDM subjects contained antibodies that precipitated GAD but inhibited its activity. Thus, overall, 21/26 (81%) preclinical and 5/13 (38%) recent-onset IDDM subjects had antibodies that precipitated GAD activity. Antibodies to GAD were not detected in sera from subjects with other autoimmune diseases (n = 29) or healthy controls (n = 14). GAD affinity-purified to homogeneity (specific activity, 58 units/mg) was specifically immunoprecipitated as a single 60-kDa species by the IDDM sera. In an ELISA incorporating whole mouse brain GAD captured by the GAD-6 monoclonal antibody the frequencies of GAD antibodies for all subject groups were indistinguishable from those found by precipitation of human brain enzymatic activity. We conclude that (i) GAD is an (auto)antigen in a majority of subjects operationally defined as having preclinical IDDM, (ii) pancreatic islet and brain GAD are likely to be cross-reactive, and (iii) the majority of GAD antibodies are directed away from the catalytic site of the brain enzyme. The lower frequency of GAD antibodies in recent-onset IDDM subjects indicates either that immunoreactivity is lost with near-total beta-cell destruction or that GAD antibodies denote a low risk of progression to clinical disease.
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