ArticleThe Journal of clinical investigation1993
Islet cell cytoplasmic autoantibody reactivity to glutamate decarboxylase in insulin-dependent diabetes.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Value of antibodies to GAD65 combined with islet cell cytoplasmic antibodies for predicting IDDM in a childhood population.Diabetologia · 1994Trial
- Antigen-specific T cell responses in autoimmune diabetes.Frontiers in immunology · 2024Review
- Proinsulin:C-peptide ratio trajectories over time in relatives at increased risk of progression to type 1 diabetes.Journal of translational autoimmunity · 2021Article
- A Type 1 Diabetes Genetic Risk Score Predicts Progression of Islet Autoimmunity and Development of Type 1 Diabetes in Individuals at Risk.Diabetes care · 2018Article
- Insulitis in Autoantibody-Positive Pancreatic Donor With History of Gestational Diabetes Mellitus.Diabetes care · 2017Article
- T Cell-Mediated Beta Cell Destruction: Autoimmunity and Alloimmunity in the Context of Type 1 Diabetes.Frontiers in endocrinology · 2017Review
- Prediction and prevention of type 1 diabetes: update on success of prediction and struggles at prevention.Pediatric diabetes · 2015Review
- Immunogenetics of type 1 diabetes mellitus.Molecular aspects of medicine · 2015Review
- Humoral autoimmunity in type 1 diabetes: prediction, significance, and detection of distinct disease subtypes.Cold Spring Harbor perspectives in medicine · 2012Review
- Islet autoantigens: structure, function, localization, and regulation.Cold Spring Harbor perspectives in medicine · 2012Review
- Antigen-specific therapeutic approaches in Type 1 diabetes.Cold Spring Harbor perspectives in medicine · 2012Review
- The pancreas in human type 1 diabetes.Seminars in immunopathology · 2011Review
- Autoimmune diabetes: ongoing development of immunological intervention strategies targeted directly against autoreactive T cells.The review of diabetic studies : RDS · 2004Article
- Intradermal skin test with diabetes specific antigens in patients with type 1 diabetes.Clinical and experimental immunology · 2001Article
- Humoral immunity against glutamic acid decarboxylase and tyrosine phosphatase IA-2 in Lambert-Eaton myasthenic syndrome.Journal of clinical immunology · 2000Article
- Comparative analysis of epitope recognition of glutamic acid decarboxylase (GAD) by autoantibodies from different autoimmune disorders.Clinical and experimental immunology · 1999Article
- Oral insulin treatment suppresses virus-induced antigen-specific destruction of beta cells and prevents autoimmune diabetes in transgenic mice.The Journal of clinical investigation · 1996Article
- Lack of agreement among two commercial enzyme-linked immunosorbent antibody assays and a conventional immunofluorescence-based method for detecting islet cell autoantibodies.Clinical and diagnostic laboratory immunology · 1996Article
- 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
- Xenografts of porcine islets immunoprotected in hollow fibres reduce the incidence of diabetes in non-obese diabetic mice.Diabetologia · 1996Article
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Authors and funding
5 authors.
Funding
Abstract
Individuals with or at risk for insulin-dependent diabetes (IDD) frequently have autoantibodies against an islet cell cytoplasmic (ICA) antigen thought to be a sialoglycolipid. However, we now report that preabsorption of ICA-positive sera with recombinant glutamate decarboxylase (human GAD 65 and/or GAD 67) reduced or blocked the ICA reactivity of 5/18 (27%) new-onset IDD patients and 7/18 (39%) prediabetics. Interestingly, nondiabetic subjects with ICA of > or = 5 yr in duration had GAD-reactive ICA significantly more often (16/24, 67%, P < 0.04) than the diabetic groups. ICA reactivity to GAD was not related to serum ICA titer nor the age of the individual, and in all cases tested was blocked by GAD 65 or GAD 67 with equivalent efficiency. The ICA observed in 21/25 (84%) IDD patients with ICA long after clinical onset of disease (9-42 yr) was reactive to GAD. A natural history analysis of three individuals showed conversions from ICA which was reactive to GAD to a non-GAD-reactive ICA nearer to their clinical onsets of IDD. This study further defines the autoantigens reactive to ICA, and suggests that, whereas ICA that are not reactive to GAD may identify an advanced and more prognostic lesion, GAD-reactive ICA may typify the early or inductive lesion that may or may not progress to clinically significant beta cell injury.
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