Erratum: Identification of the 64K autoantigen in insulin-dependent diabetes as the GABA-synthesizing enzyme glutamic acid decarboxylase

Bækkeskov, Steinunn; Aanstoot, H.J.; Stephan, Carsten; Reetz, A; Solimena, Michele; Cascalho, Marília; Folli, Franco; Richter-Oleson, Hanne; Camilli, Pietro De

doi:10.1038/347782a0

Cited by 90 publications

(24 citation statements)

References 2 publications

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“…L'antigène cible n'est pas connu avec certitude même s'il existe d'excellents candi dats, en particulier l'insuline et la glutamic acid decarboxylase (GAD) (m/s no 9, vol. 6, p. 92 1) [35][36][37] . La nature des mécanismes effecteurs reste éga lement mal définie.…”

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Peut-on rétablir la tolérance au soi dans les maladies autoimmunes ?

Chatenoud¹,

Bach²

1995

Med Sci (Paris)

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Peut-on rétablir la tolérance au soi dans les maladies autoimmunes ?

Chatenoud¹,

Bach²

1995

Med Sci (Paris)

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“…GABA may function as a paracrine signaling molecule in pancreatic islets (14). The diabetes-associated epitopes in GAD 65 are predominantly conformational and only include a linear epitope in very rare cases (5,15,16). IA2 belongs to a family of membrane-spanning tyrosine phosphatases, but its membrane compartment in ␤ cells has not yet been identified (8,9).…”

Section: Introductionmentioning

confidence: 99%

“…ICA epitopes are usually only detected on frozen but not on fixed pancreatic tissue, consistent with their conformational nature. Immunoprecipitation of islet cell lysates in the presence of nonionic detergents, which preserve the conformation of proteins, has identified the smaller form of the neuroendocrine enzyme glutamic acid decarboxylase (GAD 65 ) (5,6) and a 40-kD tryptic fragment of the tyrosine phosphatase (IA2) (7)(8)(9) as targets of islet cell antibodies associated with early as well as late stages of ␤ cell destruction in 70-80% and 50-80% of patients, respectively (5-8, and references therein). Sequence analyses of the immunoglobulin genes encoding GAD 65 autoantibodies have provided convincing evidence that the development of these antibodies is antigen driven and can involve many rounds of antigen selection (10).…”

Section: Introductionmentioning

confidence: 99%

“…The particulate membrane fraction was extracted in HEMAP buffer with 2% Triton X-114 for 2 h by repeated dispersion through a bent constricted pipette tip, followed by centrifugation at 100,000 g to remove debris. Amphiphilic proteins in both the cytosol fraction and the membrane extract were purified by temperatureinduced Triton X-114 phase separation (5). The detergent phase of either membrane or cytosol fractions was precleared with a normal human serum before immunoprecipitation with the indicated sera (21).…”

Section: Introductionmentioning

confidence: 99%

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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.

Aanstoot

Kang²,

Kim³

et al. 1996

J. Clin. Invest.

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Immunoprecipitating IgG autoantibodies to glutamic acid decarboxylase, GAD 65 , and/or a tyrosine phosphatase, IA2, are present in the majority of individuals experiencing pancreatic ␤ 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 GAD 65 and IA2. Removal of N-linked carbohydrates results in a protein of 22,000 M r . 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 GAD 65 and glima 38 antibodies in these two groups was 83 and 80%, respectively, and the cumulative incidence of GAD 65

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“…High titered ICA, their presence in children rather than in adults, and the additional presence of insulin autoantibodies (IAA) in the sera of such patients all increase the risk of IDD associated with ICA (4)(5)(6)(7)(8)(9). Autoantibodies to the 64,000-M, islet cell protein (recently identified to be the lower molecular weight isoform ofglutamic acid decarboxylase [GAD65]) are the most often detectable autoantibodies before diagnosis( IO, 11).…”

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confidence: 99%

Islet cell antibodies predict insulin-dependent diabetes in United States school age children as powerfully as in unaffected relatives.

Schatz¹,

Krischer²,

Horne³

et al. 1994

J. Clin. Invest.

129

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IntroductionIslet cell antibodies (ICA) in the sera of nondiabetic relatives of patients with insulin-dependent diabetes (IDD) are predictive of the disease, a finding that permits the design of intervention strategies to prevent it. However, 85% or more of patients with new onset IDD have no affected relative. We therefore screened 9,696 schoolchildren between the ages of 5 and 18 yr (mean age 10.7 yr) in Pasco County, Florida for ICA in three surveys during 1984/5, 1987/8, and 1990/1 and have followed them prospectively. Approximately 4,000 of these children have been followed for nearly 8 yr. ICA titers 2 10 Juvenile Diabetes Foundation units on replicate tests were detected in 57 of the children (0.59%). 10 children have developed diabetes so far, and all had ICA detected beforehand. The likelihood of developing IDD among the ICA-positive children was compared with 2,959 age-matched nondiabetic first degree relatives of IDD probands who were screened for ICA by our laboratory during the same time period and also followed prospectively. Of 103 (3.5%) ICA-positive relatives, 31 have developed IDD. Life table analysis reveals no statistically significant differences in the probability of developing IDD between the ICApositive schoolchildren and ICA-positive first degree relatives (P = 0.3). The estimated risk of developing IDD by 7 yr in the ICA-positive schoolchildren was 45% (95% confidence interval 15-74%) compared with 43% (confidence interval 22-63%) in the relatives. We conclude that ICA appear to be as predictive of IDD in low-risk schoolchildren as they are in high-risk relatives. These data suggest that it is feasible to predict IDD by screening a general population of schoolchildren for ICA and that those found to be positive could be considered, in addition to relatives, for intervention protocols to prevent the disease.

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Erratum: Identification of the 64K autoantigen in insulin-dependent diabetes as the GABA-synthesizing enzyme glutamic acid decarboxylase

Cited by 90 publications

References 2 publications

Peut-on rétablir la tolérance au soi dans les maladies autoimmunes ?

Peut-on rétablir la tolérance au soi dans les maladies autoimmunes ?

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.

Islet cell antibodies predict insulin-dependent diabetes in United States school age children as powerfully as in unaffected relatives.

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