Jun H S, Yoon J W
Julia McFarlane Diabetes Research Centre, University of Calgary, Alberta.
Adv Exp Med Biol. 1994;347:207-20. doi: 10.1007/978-1-4615-2427-4_18.
Insulin-dependent diabetes mellitus (IDDM) is believed to be an autoimmune disease, characterized by lymphocytic infiltration of the islets and the presence of islet cell autoantibodies. Autoimmunity may result from an intrinsically abnormal immune system, primary alterations of the target beta cell or both. However, the initial event that causes the beta cell-specific autoimmunity remains unknown. Our recent experimental results showed that islet grafts from neonatal BB rats remained intact without insulitis when transplanted into the renal subcapsular space of acutely diabetic BB rats. In contrast, islet grafts from adult BB rats (which had been treated with silica for the prevention of insulitis) revealed severe insulitis and were rapidly destroyed. These results suggest that the delayed expression of a beta cell-specific autoantigen may result in the initiation of beta cell-specific autoimmunity. The islet cell-specific 37 kd autoantigen is not expressed early in the life of BB rats, but is expressed at around 30 days of age. This islet-specific autoantigen might be recognized and attacked by the immune effectors. In contrast, nondiabetic Wistar Furth rats express the autoantigen from birth.
胰岛素依赖型糖尿病（IDDM）被认为是一种自身免疫性疾病，其特征是胰岛出现淋巴细胞浸润以及存在胰岛细胞自身抗体。自身免疫可能源于内在异常的免疫系统、靶β细胞的原发性改变或两者皆有。然而，引发β细胞特异性自身免疫的初始事件仍不清楚。我们最近的实验结果表明，将新生BB大鼠的胰岛移植到急性糖尿病BB大鼠的肾被膜下间隙时，胰岛移植体保持完整且无胰岛炎。相反，成年BB大鼠（已用二氧化硅处理以预防胰岛炎）的胰岛移植体则出现严重的胰岛炎并迅速被破坏。这些结果表明β细胞特异性自身抗原的延迟表达可能导致β细胞特异性自身免疫的启动。胰岛细胞特异性37kd自身抗原在BB大鼠生命早期不表达，但在约30日龄时表达。这种胰岛特异性自身抗原可能会被免疫效应器识别并攻击。相比之下，非糖尿病的Wistar Furth大鼠从出生起就表达该自身抗原。
