Abstract
Recent headlines in the national and presumably international news media have characterized the enzyme glutamic acid decarboxylase (GAD) as the cause of type I diabetes. The news accounts were stimulated by two excellent research reports that indicated that Tcells from the spleens of young NOD mice responded to GAD before other autoantigens and that intravenous injection of GAD or intrathymic injection of GAD prevented the development of diabetes (1,2).
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