Huang X, Hultgren B, Dybdal N, Stewart T A
Department of Endocrine Research, Genentech, Incorporated, South San Francisco, California 94080.
Immunity. 1994 Sep;1(6):469-78. doi: 10.1016/1074-7613(94)90089-2.
The mechanism(s) leading to beta cell dysfunction in type I diabetes has not been defined. We have investigated whether islet expression of IFN alpha could be a cause of the lesions that are hallmarks of type I diabetes. Streptozotocin induces the expression of interferon-alpha by pancreatic islets prior to the diabetes induced by streptozotocin. Increased IFN alpha, induced by poly I/C or expressed from a transgene will exacerbate the diabetogenic effects of streptozotocin. In another rodent model of type I diabetes (the BB rat), islet expression of IFN alpha precedes lymphocytic infiltration and diabetes. As in the streptozotocin model, in the BB rats poly I/C will induce islet expression of IFN alpha and accelerate the onset of diabetes. These results are consistent with the hypothesis that islet expression of IFN alpha participates in causing type I diabetes.
导致I型糖尿病中β细胞功能障碍的机制尚未明确。我们研究了胰岛中IFNα的表达是否可能是I型糖尿病标志性病变的一个原因。链脲佐菌素在由其诱导的糖尿病发生之前，会诱导胰岛表达干扰素α。由聚肌胞苷酸（poly I/C）诱导增加的IFNα或从转基因表达的IFNα会加剧链脲佐菌素的致糖尿病作用。在I型糖尿病的另一种啮齿动物模型（BB大鼠）中，胰岛中IFNα的表达先于淋巴细胞浸润和糖尿病出现。与链脲佐菌素模型一样，在BB大鼠中聚肌胞苷酸会诱导胰岛表达IFNα并加速糖尿病的发病。这些结果与IFNα在胰岛中的表达参与导致I型糖尿病这一假说相符。
