Vialettes B, Baume D, Charpin C, De Maeyer-Guignard J, Vague P
J Clin Lab Immunol. 1983 Jan;10(1):35-40.
EMC virus-induced diabetes in mice may be a model of human type I diabetes. It is postulated that auto-immune reaction plays a role in beta cell destruction after viral aggression. The use of anti-viral (interferon) or immunosuppressive drugs (Cyclosporin A) could contribute to an understanding of the pathogenesis of diabetes in this model. Early or late administration of cyclosporin A increased mortality and frequency of diabetes in female mice and did not influence these parameters in males despite a reduction of pancreatic inflammatory lesions. Interferon administered at the time of virus inoculation diminished mortality in both sexes and frequency of diabetes in males. These results are against an autoimmune pathogenesis for diabetes in this model and suggest that the virus plays the major role in beta cell damage.
脑心肌炎病毒诱导的小鼠糖尿病可能是人类I型糖尿病的一种模型。据推测,自身免疫反应在病毒侵袭后β细胞破坏过程中起作用。使用抗病毒药物(干扰素)或免疫抑制药物(环孢素A)可能有助于理解该模型中糖尿病的发病机制。早期或晚期给予环孢素A会增加雌性小鼠的死亡率和糖尿病发生率,尽管胰腺炎症病变有所减轻,但对雄性小鼠的这些参数没有影响。在接种病毒时给予干扰素可降低两性的死亡率以及雄性小鼠的糖尿病发生率。这些结果与该模型中糖尿病的自身免疫发病机制相悖,并表明病毒在β细胞损伤中起主要作用。