Wicker L S, Leiter E H, Todd J A, Renjilian R J, Peterson E, Fischer P A, Podolin P L, Zijlstra M, Jaenisch R, Peterson L B
Department of Autoimmune Diseases Research, Merck Research Laboratories, Rahway, New Jersey 07065-0900.
Diabetes. 1994 Mar;43(3):500-4. doi: 10.2337/diab.43.3.500.
The role of CD8+ T-cells in the development of diabetes in the nonobese diabetic (NOD) mouse remains controversial. Although it is widely agreed that class II-restricted CD4+ T-cells are essential for the development of diabetes in the NOD model, some studies have suggested that CD8+ T-cells are not required for beta-cell destruction. To assess the contribution of CD8+ T-cells to diabetes, we have developed a class of NOD mouse that lacks expression of beta 2-microglobulin (NOD-B2mnull). NOD-B2mnull mice, which lack both class I expression and CD8+ T-cells in the periphery, not only failed to develop diabetes but were completely devoid of insulitis. These results demonstrate an essential role for CD8+ T-cells in the initiation of the autoimmune response to beta-cells in the NOD mouse.
CD8 + T细胞在非肥胖糖尿病（NOD）小鼠糖尿病发病过程中的作用仍存在争议。尽管人们普遍认为，II类限制性CD4 + T细胞对于NOD模型中糖尿病的发病至关重要，但一些研究表明，β细胞破坏并不需要CD8 + T细胞。为了评估CD8 + T细胞对糖尿病的影响，我们培育出了一类缺乏β2-微球蛋白表达的NOD小鼠（NOD - B2mnull）。外周既缺乏I类分子表达又缺乏CD8 + T细胞的NOD - B2mnull小鼠不仅不会患糖尿病，而且完全没有胰岛炎。这些结果证明了CD8 + T细胞在NOD小鼠针对β细胞的自身免疫反应启动过程中起着至关重要的作用。
