Yoshida K, Kikutani H
Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Japan.
Rev Immunogenet. 2000;2(1):140-6.
The non-obese diabetic (NOD) mouse is an animal model of human insulin-dependent diabetes mellitus (IDDM). Most NOD mice show insulitis at several weeks of age, and 60-90% of the female mice develop overt diabetes after 20-30 weeks of age. NOD mice share many features of human IDDM. As in human IDDM, the disease development in NOD mice is controlled by a number of disease susceptibility or resistant genes (Idds), including the major histocompatibility complex locus. Cumulative evidence suggests that Thl CD4+ T cells play a critical role in the autoimmune process leading to beta cell destruction. In addition to CD4+ T cells, CD8+ cells and B cells also participate in the pathogenesis. There are several candidate antigens recognized by autoreactive T cells such as glutamic acid decarboxylase (GAD), insulin and heat shock protein (HSP) 60. Treatment by these antigens suppresses IDDM development in NOD mice, suggesting that they may initiate the autoimmune process of NOD mice.
非肥胖型糖尿病（NOD）小鼠是人类胰岛素依赖型糖尿病（IDDM）的一种动物模型。大多数NOD小鼠在几周龄时会出现胰岛炎，60%-90%的雌性小鼠在20-30周龄后会发展为显性糖尿病。NOD小鼠具有人类IDDM的许多特征。与人类IDDM一样，NOD小鼠的疾病发展受许多疾病易感或抗性基因（Idds）控制，包括主要组织相容性复合体基因座。越来越多的证据表明，Th1 CD4+ T细胞在导致β细胞破坏的自身免疫过程中起关键作用。除了CD4+ T细胞外，CD8+细胞和B细胞也参与发病机制。有几种自身反应性T细胞识别的候选抗原，如谷氨酸脱羧酶（GAD）、胰岛素和热休克蛋白（HSP）60。用这些抗原进行治疗可抑制NOD小鼠IDDM的发展，这表明它们可能引发NOD小鼠的自身免疫过程。
