非肥胖糖尿病（NOD）小鼠β细胞自身免疫的免疫遗传学分析。胰岛炎与T淋巴细胞受体β链NOD基因和Aβ链NOD基因的关系。

Immunogenetic analysis of beta-cell autoimmunity in NOD mice. Relationship of insulitis to T-lymphocyte-receptor beta nod and A beta nod genes.

作者信息

Winter W E, Shimpo K, Obata M, Yamada K, Luchetta R

机构信息

Department of Pathology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville 32610.

出版信息

Diabetes. 1990 Aug;39(8):975-82. doi: 10.2337/diab.39.8.975.

DOI:10.2337/diab.39.8.975

PMID:1973674

Abstract

An early molecular event in the evolution of insulin-dependent diabetes in humans and NOD mice appears to involve the interaction of MHC class II molecules, beta-cell autoantigen-derived peptides, and receptor molecules of helper T lymphocytes. To examine the influence of T-lymphocyte-receptor beta-genes on the development of beta-cell autoimmunity, (NOD x NZW)F1 x NOD backcrossed (BC) mice were studied for the development of insulitis, because insulitis is the pathognomonic histological lesion of autoimmune diabetes. Heterozygosity for H-2nod was permissive for the development of pancreatic interstitial inflammation and peri-islet insulitis, whereas homozygosity for H-2nod was highly associated with insulitis. However, (NOD x NZW)F1 x NOD BC mice developed insulitis regardless of homozygosity or heterozygosity for T-lymphocyte receptor beta nod. Therefore, in our study, T-lymphocyte receptor beta nod did not function as an autosomal-recessive beta-cell autoimmunity gene.

摘要

在人类和非肥胖糖尿病（NOD）小鼠胰岛素依赖型糖尿病的早期分子事件中，似乎涉及到MHC II类分子、β细胞自身抗原衍生肽以及辅助性T淋巴细胞受体分子之间的相互作用。为了研究T淋巴细胞受体β基因对β细胞自身免疫发展的影响，对（NOD×NZW）F1×NOD回交（BC）小鼠进行了胰岛炎发展情况的研究，因为胰岛炎是自身免疫性糖尿病的特征性组织学病变。H-2nod杂合性有利于胰腺间质炎症和胰岛周围胰岛炎的发展，而H-2nod纯合性与胰岛炎高度相关。然而，（NOD×NZW）F1×NOD BC小鼠无论T淋巴细胞受体βnod是纯合还是杂合都会发生胰岛炎。因此，在我们的研究中，T淋巴细胞受体βnod不作为常染色体隐性β细胞自身免疫基因发挥作用。