ArticleThe Journal of clinical investigation1996
Identification and characterization of glima 38, a glycosylated islet cell membrane antigen, which together with GAD65 and IA2 marks the early phases of autoimmune response in type 1 diabetes.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 92 citations in OpenAlex.
- Autoimmunity to tetraspanin-7 in type 1 diabetes.Medical microbiology and immunology · 2020Review
- GAD antibodies in neurological disorders - insights and challenges.Nature reviews. Neurology · 2020Review
- Birth and coming of age of islet autoantibodies.Clinical and experimental immunology · 2019Review
- Tetraspanin 7 autoantibodies predict progressive decline of beta cell function in individuals with LADA.Diabetologia · 2019Article
- Tetraspanin 7 autoantibodies in type 1 diabetes.Diabetologia · 2016Article
- Novel biomarkers in type 1 diabetes.The review of diabetic studies : RDS · 2012Review
- An update on the use of NOD mice to study autoimmune (Type 1) diabetes.Expert review of clinical immunology · 2010Article
- Approaches in type 1 diabetes research: A status report.International journal of diabetes in developing countries · 2009Article
- Autoimmune diabetes: ongoing development of immunological intervention strategies targeted directly against autoreactive T cells.The review of diabetic studies : RDS · 2004Article
- Review
- Evaluation of the new ADA and WHO criteria for classification of diabetes mellitus in young adult people (15-34 yrs) in the Diabetes Incidence Study in Sweden (DISS).Diabetologia · 2003Article
- The diabetes autoantigen ICA69 and its Caenorhabditis elegans homologue, ric-19, are conserved regulators of neuroendocrine secretion.Molecular biology of the cell · 2000Article
- Multiple genes/multiple autoantigens role in type 1 diabetes.Clinical reviews in allergy & immunology · 2000Review
- Treatment of an autoimmune disease with "classical" T cell veto: a proposal.Journal of clinical immunology · 1999Review
- T-cell response to proinsulin and insulin in type 1 and pretype 1 diabetes.Journal of clinical immunology · 1999Article
- Encephalitogenicity of myelin-associated oligodendrocytic basic protein and 2',3'-cyclic nucleotide 3'-phosphodiesterase for BALB/c and SJL mice.Immunology · 1998Article
- An islet-cell protein tyrosine phosphatase is a likely precursor to the 37-kDa autoantigen in type 1 diabetes: human and macaque sequences, tissue distribution, unique and shared epitopes, and predictive autoantibodies.Molecular medicine (Cambridge, Mass.) · 1997Article
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15 authors at 7 institutions in 6 countries.
Funding
Abstract
Immunoprecipitating IgG autoantibodies to glutamic acid decarboxylase, GAD65, and/or a tyrosine phosphatase, IA2, are present in the majority of individuals experiencing pancreatic beta cell destruction and development of type 1 diabetes. Here we identify a third islet cell autoantigen, a novel 38-kD protein, which is specifically immunoprecipitated with sera from a subset of prediabetic individuals and newly diagnosed type 1 diabetic patients. The 38-kD autoantigen, named glima 38, is an amphiphilic membrane glycoprotein, specifically expressed in islet and neuronal cell lines, and thus shares the neuroendocrine expression patterns of GAD65 and IA2. Removal of N-linked carbohydrates results in a protein of 22,000 Mr. Glima 38 autoantibodies were detected in 16/86 (19%) of newly diagnosed patients, including three very young children, who had a rapid onset of disease, and in 6/44 (14%) of prediabetic individuals up to several years before clinical onset. The cumulative incidence of GAD65 and glima 38 antibodies in these two groups was 83 and 80%, respectively, and the cumulative incidence of GAD65, glima 38, and IA2 antibodies in the same groups was 91 and 84%, respectively. GAD65, IA2, and glima 38 represent three distinct targets of immunoprecipitating IgG autoantibodies associated with beta cell destruction and type 1 diabetes.
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