Sumida T, Furukawa M, Sakamoto A, Namekawa T, Maeda T, Zijlstra M, Iwamoto I, Koike T, Yoshida S, Tomioka H
Second Department of Internal Medicine, School of Medicine, Chiba University, Japan.
Int Immunol. 1994 Sep;6(9):1445-9. doi: 10.1093/intimm/6.9.1445.
beta 2-Microglobulin (beta 2m)-deficient non-obese diabetic (NOD) mice were established by crossing beta 2m-deficient 129/Sv mice with NOD mice, and used to examine the possible involvement of MHC class I molecules and CD8+ T cells in the development of insulitis and diabetes. In these mice, MHC class I molecules were not expressed, resulting in no generation of CD8+ T cells. None of eight lines of beta 2m-deficient NOD mice (-/-) established developed overt diabetes by 32 weeks, while control littermates (+/+) became diabetic by 22 weeks. histological studies showed no significant lymphocyte infiltration of the islets (insulitis score: 0.03 +/- 0.03) in any of the beta 2m-deficient NOD mice (-/-) compared with littermate NOD mice (+/+) with overt insulitis (1.42 +/- 0.28). These findings support the notion that the expression of MHC class I molecules and/or CD8+ T cells plays an essential role in the infiltration of CD4+ T cells in islets as well as the development of diabetes in NOD mice.
通过将β2微球蛋白（β2m）缺陷的129/Sv小鼠与非肥胖糖尿病（NOD）小鼠杂交，建立了β2m缺陷的NOD小鼠，并用于研究MHC I类分子和CD8 + T细胞在胰岛炎和糖尿病发展中可能的作用。在这些小鼠中，MHC I类分子不表达，导致CD8 + T细胞无法产生。8个品系的β2m缺陷NOD小鼠（-/-）在32周时均未发生明显的糖尿病，而对照同窝小鼠（+/+）在22周时出现糖尿病。组织学研究表明，与有明显胰岛炎（1.42 +/- 0.28）的同窝NOD小鼠（+/+）相比，任何β2m缺陷的NOD小鼠（-/-）的胰岛均无明显的淋巴细胞浸润（胰岛炎评分：0.03 +/- 0.03）。这些发现支持了这样的观点，即MHC I类分子和/或CD8 + T细胞的表达在NOD小鼠胰岛中CD4 + T细胞的浸润以及糖尿病的发展中起着至关重要的作用。
