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通过II类主要组织相容性复合体和γ干扰素的异位表达在转基因小鼠中诱导产生胰岛素依赖型糖尿病。

Insulin-dependent diabetes mellitus induced in transgenic mice by ectopic expression of class II MHC and interferon-gamma.

作者信息

Sarvetnick N, Liggitt D, Pitts S L, Hansen S E, Stewart T A

机构信息

Department of Developmental Biology, Genentech, Inc., South San Francisco, California 94080.

出版信息

Cell. 1988 Mar 11;52(5):773-82. doi: 10.1016/0092-8674(88)90414-x.

Abstract

We have produced transgenic mouse strains harboring class II major histocompatibility complex or interferon-gamma genes linked to the human insulin promoter. These experiments were designed to investigate the consequences of the expression of immunological effector molecules by nonimmunological cells. In both of these studies we observed the disappearance from the pancreas of the insulin-producing beta cells coinciding with the development of insulin-dependent diabetes mellitus. Transgenic mice expressing both chains of the I-A gene showed progressive atrophy of the islets of Langerhans, whereas mice expressing interferon-gamma suffered an inflammatory destruction of the islets.

摘要

我们已培育出携带与人类胰岛素启动子相连的II类主要组织相容性复合体或干扰素-γ基因的转基因小鼠品系。这些实验旨在研究非免疫细胞表达免疫效应分子的后果。在这两项研究中,我们均观察到胰岛素生成β细胞从胰腺中消失,这与胰岛素依赖型糖尿病的发展相一致。表达I-A基因两条链的转基因小鼠出现胰岛渐进性萎缩,而表达干扰素-γ的小鼠胰岛遭受炎性破坏。

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