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1A型糖尿病的细胞与分子发病机制

Cellular and molecular pathogenesis of type 1A diabetes.

作者信息

Jahromi M M, Eisenbarth G S

机构信息

Barbara Davis Center for Childhood Diabetes, University of Colorado, Health sciences Center, Aurora, CO 80010, USA.

出版信息

Cell Mol Life Sci. 2007 Apr;64(7-8):865-72. doi: 10.1007/s00018-007-6469-4.

DOI:10.1007/s00018-007-6469-4
PMID:17429581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11136453/
Abstract

Type 1A diabetes is an organ-specific autoimmune disease resulting from destruction of insulin-producing pancreatic beta-cells. The main susceptibility genes code for polymorphic HLA molecules and in particular alleles of class II MHC genes (DR, DQ and DP). Polymorphisms of individual genes outside the MHC also contribute to diabetes risk but recent evidence suggests that there are additional non-HLA genes determining susceptibility linked to the MHC. It is now possible using genetic and autoantibody assays to predict the development of type 1A diabetes in the majority of individuals, and trials of diabetes prevention are underway.

摘要

1A型糖尿病是一种器官特异性自身免疫性疾病,由产生胰岛素的胰腺β细胞被破坏所致。主要的易感基因编码多态性HLA分子,尤其是II类MHC基因(DR、DQ和DP)的等位基因。MHC之外的单个基因的多态性也会增加患糖尿病的风险,但最近的证据表明,还有其他与MHC相关的非HLA基因决定易感性。现在利用基因和自身抗体检测能够在大多数个体中预测1A型糖尿病的发生,并且糖尿病预防试验正在进行中。