Gould C L, McMannama K G, Bigley N J, Giron D J
Diabetes. 1985 Dec;34(12):1217-21. doi: 10.2337/diab.34.12.1217.
Adult, male ICR Swiss mice are susceptible to the diabetogenic effects of the D-variant of encephalomyocarditis virus (EMC-D) in contrast to adult C3H/HeJ male mice, which are relatively resistant. To date, experimental evidence suggests that the immune system plays a role in the pathogenesis of this infection. We have investigated the potential involvement of the immune system in the pathogenesis of EMC-D-induced diabetes using cyclosporin-A (CyA), a potent immunosuppressive drug. The data show that treatment with CyA results in increased severity and incidence of diabetes in susceptible ICR Swiss mice and induction of diabetes in resistant C3H/HeJ mice. It is concluded that immune mediation probably is not involved in the early pathogenesis of EMC-D-induced diabetes in mice.
成年雄性ICR瑞士小鼠易受脑心肌炎病毒D变种(EMC-D)的致糖尿病作用影响,而成年C3H/HeJ雄性小鼠则相对具有抗性。迄今为止,实验证据表明免疫系统在这种感染的发病机制中起作用。我们使用强效免疫抑制药物环孢素A(CyA)研究了免疫系统在EMC-D诱导的糖尿病发病机制中的潜在作用。数据显示,用CyA治疗会导致易感的ICR瑞士小鼠糖尿病的严重程度和发病率增加,并使抗性C3H/HeJ小鼠诱发糖尿病。得出的结论是,免疫介导可能不参与小鼠EMC-D诱导的糖尿病的早期发病机制。