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Species-Specific Autoantibodies in Type 1 Diabetes¹

Department of Medicine, University of Washington (C.S.H., D.B.S., A.L.), Seattle, Washington 98195; and the Department of Medicine, University Hospital (M.L.-O., C.T.), Lund; the Department of Family Medicine, Umea University (O.R., A.A.), Umea; and the Department of Woman and Child Health, Karolinska Institute (E.O., B.P.), Stockholm, Sweden

Address all correspondence and requests for reprints to: Dr. Christiane S. Hampe, Department of Medicine, Box 357710, University of Washington, Seattle, Washington 98195. E-mail: champe{at}u

GAD65 autoantibodies (GAD65Ab) are important markers for type 1 (insulin-dependent) diabetes mellitus. Although most patients have GAD65Ab at the time of clinical diagnosis, there are also GAD65Ab-positive individuals in the population at low risk of developing type 1 diabetes. The aim of this study was to test the hypothesis that the GAD65Ab reactivity to GAD65 cloned from human, mouse, and rat in newly diagnosed type 1 diabetic patients differ from antibody-positive healthy individuals. Sera from 254 new-onset 0- to 34-yr-old type 1 diabetic patients and 270 controls were assayed for their reactivity to human, mouse, and rat GAD65. Among the type 1 diabetic patients there was a significant better binding of human GAD65 compared to either mouse (P = 0.03) or rat GAD65 (P = 0.0005). The preference for human GAD65 increased with increasing age at onset (P = 0.0002). This differentiation was not observed in 88 GAD65Ab-positive control subjects. Our data indicate that recognition of epitopes by GAD65Ab in type 1 diabetes is different from that in nontype 1 diabetes, GAD65Ab-positive individuals.

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