ISLET EXPRESSION OF INTERFERON-ALPHA PRECEDES DIABETES IN BOTH THE BB RAT AND STREPTOZOTOCIN-TREATED MICE
ISLET EXPRESSION OF INTERFERON-ALPHA PRECEDES DIABETES IN BOTH THE BB RAT AND STREPTOZOTOCIN-TREATED MICE
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DOI：
10.1016/1074-7613(94)90089-2
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发表时间：
1994-09-01
期刊：
影响因子：
32.4
通讯作者：
STEWART, TA
中科院分区：
文献类型：
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作者：
HUANG, XJ;HULTGREN, B;STEWART, TA
导致I型糖尿病中β细胞功能障碍的机制尚未确定。我们已经研究了胰岛表达IFN α是否可能是I型糖尿病标志性病变的原因。链脲佐菌素诱导糖尿病前胰岛表达α-干扰素。由聚I/C诱导或由转基因表达的IFN α增加将加剧链脲佐菌素的致糖尿病作用。在另一种I型糖尿病啮齿动物模型（BB大鼠）中，IFN α的胰岛表达先于淋巴细胞浸润和糖尿病。如在链脲佐菌素模型中，在BB大鼠中聚I/C将诱导IFN α的胰岛表达并加速糖尿病的发作。这些结果与IFN α的胰岛表达参与引起I型糖尿病的假设一致。
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.