由于胰腺β细胞中I类组织相容性分子过度表达导致的转基因小鼠糖尿病。
Diabetes in transgenic mice resulting from over-expression of class I histocompatibility molecules in pancreatic beta cells.
作者信息
Allison J, Campbell I L, Morahan G, Mandel T E, Harrison L C, Miller J F
机构信息
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
出版信息
Nature. 1988 Jun 9;333(6173):529-33. doi: 10.1038/333529a0.
DOI:10.1038/333529a0
PMID:3287175
Abstract
A class I histocompatibility gene, H-2Kb, linked to the rat insulin promoter, is overexpressed in the pancreatic beta cells of transgenic mice. The mice, whether syngeneic or allogeneic to the transgene, develop insulin dependent diabetes without detectable T cell infiltration, suggesting a direct, non-immune role for the transgenic class I molecules in the disease process.
摘要
与大鼠胰岛素启动子相连的I类组织相容性基因H-2Kb在转基因小鼠的胰腺β细胞中过度表达。这些小鼠，无论与转基因是同基因还是异基因，都会发展为胰岛素依赖型糖尿病，且未检测到T细胞浸润，这表明转基因I类分子在疾病过程中发挥直接的非免疫作用。
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