作者: J. M. Jasinski , G. S. Eisenbarth
DOI: 10.1080/17402520500078204
关键词:
摘要: Type 1A diabetes mellitus is caused by specific and progressive autoimmune destruction of the beta cells in islets Langerhans whereas other cell types islet (alpha, delta, PP) are spared. The autoantigens may be divided into subgroups based on their tissue distributions: Beta-cell-specific antigens like insulin, insulin derivatives, IGRP (Islet-specific Glucose-6-phosphatase catalytic subunit Related Peptide); neurendocrine such as carboxypeptidase H, insulinoma-associated antigen (IA-2), glutamic acid decarboxylase (GAD65), E; those expressed ubiquitously heat shock protein 60 (a putative autoantigen for type 1 diabetes). This review will focus specifically a primary autoantigen, an essential target disease, mellitus. In particular, immunization with peptide B:9-23 can used to induce autoantibodies animal models or prevent diabetes. Genetic manipulation 2 genes reciprocally alters development NOD mouse, gene polymorphisms important determinants childhood We pursuing hypothesis that diabetes, thus pathogenesis disease relates recognition one more peptides.