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Titolo:
Recognition of glutamic acid decarboxylase (GAD) by autoantibodies from different GAD antibody-positive phenotypes
Autore:
Hampe, CS; Hammerle, LP; Bekris, L; Ortqvist, E; Kockum, I; Rolandsson, O; Landin-Olsson, M; Torn, C; Persson, B; Lernmark, A;
Indirizzi:
Univ Washington, Dept Med, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 ton, Dept Med, Seattle, WA 98195 USA Karolinska Inst, Dept Mol Med, S-17176 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-17176 Med, S-17176 Stockholm, Sweden Umea Univ, Dept Publ Hlth & Clin Med, S-90187 Umea, Sweden Umea Univ Umea Sweden S-90187 Publ Hlth & Clin Med, S-90187 Umea, Sweden Univ Hosp, Dept Med, S-22100 Lund, Sweden Univ Hosp Lund Sweden S-22100Univ Hosp, Dept Med, S-22100 Lund, Sweden Karolinska Inst, Dept Woman & Child Hlth, S-17176 Stockholm, Sweden Karolinska Inst Stockholm Sweden S-17176 Hlth, S-17176 Stockholm, Sweden
Titolo Testata:
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
fascicolo: 12, volume: 85, anno: 2000,
pagine: 4671 - 4679
SICI:
0021-972X(200012)85:12<4671:ROGAD(>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT DIABETES-MELLITUS; ISLET-CELL-ANTIBODIES; SYNDROME TYPE-I; IA-2 AUTOANTIBODIES; DIFFERENT EPITOPES; CHILDHOOD IDDM; ISOFORM; CLONING; ONSET; ASSAY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Hampe, CS Univ Washington, Dept Med, Box 357710, Seattle, WA 98195 USA Univ Washington Box 357710 Seattle WA USA 98195 le, WA 98195 USA
Citazione:
C.S. Hampe et al., "Recognition of glutamic acid decarboxylase (GAD) by autoantibodies from different GAD antibody-positive phenotypes", J CLIN END, 85(12), 2000, pp. 4671-4679

Abstract

Autoantibodies against the smaller isoform of glutamic acid decarboxylase (GAD) are markers for Type 1 diabetes. GAD65 autoantibody (GAD65Ab)-positive individuals in the general population are, however, mostly at low risk ofdeveloping Type 1 diabetes, suggesting that GAD65Ab phenotypes may be associated with different underlying pathogenic processes. The aim of this study was to test the hypothesis that Type 1 diabetes patients (n = 243; group I), GAD65Ab-positive healthy individuals (n = 28; group II), and healthy first-degree relatives of Type 1 diabetes patients (n = 41; group III) have antibody phenotypes that recognize different GAD65 epitopes. Sera from groups I-III were tested for their binding to GAD65 and GAD67, as well as six different GAD65/67 fusion proteins. Regardless of group, sera reactive to both GAD65 and GAD67 showed broader epitope reactivity than GAD65-specific sera. Furthermore, Type 1 diabetes patients showed a more restricted epitope binding than healthy individuals and first-degree relatives, demonstrating significantly less binding to the N-terminal part of GAD65 and to GAD67. Ouranalysis demonstrates that the N-terminal part is essential for full antibody binding to GAD65, in particular, to the middle epitope. It is suggestedthat Type 1 diabetes is associated with restricted GAD65Ab epitope specificity.

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Documento generato il 01/12/20 alle ore 01:18:11