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实验动物中糖尿病诱导的免疫学研究。链脲佐菌素诱导糖尿病的细胞基础。

Immunologic studies on the induction of diabetes in experimental animals. Cellular basis for the induction of diabetes by streptozotocin.

作者信息

Kim Y T, Steinberg C

出版信息

Diabetes. 1984 Aug;33(8):771-7. doi: 10.2337/diab.33.8.771.

DOI:10.2337/diab.33.8.771
PMID:6235141
Abstract

Repeated low doses of streptozotocin (STZ, 40 mg/kg body wt) gradually induce hyperglycemia in mice after a latent period of 5-7 days. The ability of STZ to induce hyperglycemia varies in different mouse strains. Repeated low doses of STZ fail to induce diabetes in T-cell-deficient mice, suggesting a crucial role of T-cells in the induction of diabetes by this procedure. Transfer of spleen cells from mice rendered diabetic by repeated low doses of STZ failed to induce hyperglycemia in the recipients. However, pretreating the recipients with a single low dose of STZ permitted efficient transfer of the diabetic state, suggesting that the immunologic reaction resulting in diabetes was actually specific for an STZ-modified beta cell.

摘要

重复低剂量链脲佐菌素(STZ,40毫克/千克体重)在5至7天的潜伏期后可逐渐诱导小鼠出现高血糖症。STZ诱导高血糖症的能力在不同小鼠品系中有所不同。重复低剂量的STZ无法在T细胞缺陷小鼠中诱导糖尿病,这表明T细胞在此诱导糖尿病过程中起关键作用。将经重复低剂量STZ诱导成糖尿病的小鼠的脾细胞转移至受体小鼠中,未能诱导受体小鼠出现高血糖症。然而,先用单次低剂量STZ预处理受体小鼠,则可有效地转移糖尿病状态,这表明导致糖尿病的免疫反应实际上对经STZ修饰的β细胞具有特异性。

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