Expression of glutamic acid decarboxylase (GAD) and its role as an autoantigen in insulin-dependent diabetes
作者： Beverly E. Faulkner-Jones , Michelle B. French , Robert S. Schmidli , Susan Williamson , David S. Cram
DOI: 10.1007/978-1-4612-4112-6_1
关键词:
摘要: Insulin-dependent diabetes mellitus (IDDM) results from autoimmune, T-lym-phocyte-dependent destruction of pancreatic islet B-cells in the two rodent models human IDDM, non-obese diabetic (NOD) mouse and Bio-Breeding (BB) rat.1,2 Similar pathogenic mechanisms are thought to result IDDM.3 In all three species, autoimmune B-cell appears be a highly selective process, with relative sparing other cell types. The primary target antigen and/or presentation antigenic peptide is thus likely either unique B-cell, or at least B-cell-restricted within islets.3
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