中文摘要：

目的探讨1型糖尿病（T1DM）小鼠胰岛表达CD68、CD22的改变,血清白介素-12（IL-12）、白介素-4（IL-4）水平的变化及可能的机制。方法正常雄性C57BL/6J小鼠104只,随机分为正常对照组、盐水对照组及实验组。小剂量多次注射链脲佐菌素（MLD-STZ）建立1型糖尿病小鼠模型,分别于第3、7、10、14、21、28天测空腹血糖,取胰尾组织及血清,通过免疫组化SABC法、酶联免疫吸附法（ELISA）及形态计量法进行研究。结果与正常及盐水对照组相比较,实验组小鼠胰岛数目减少,胰岛面积减小。实验组小鼠胰岛CD68阳性细胞的面数密度（NA）于第3天起明显高于正常对照组和盐水对照组（P〈0.01）,但第10天的NA在实验组相对较低。实验组胰岛CD22阳性细胞的NA值于第3天即高于正常对照组和盐水对照组（P〈0.01）,至第7天最高。血清ELISA结果显示,实验组小鼠血清IL-12水平自第7天开始增高（P〈0.05）;而血清IL-4水平与正常及盐水对照组相比有所降低,差异有统计学意义（P〈0.05）。结论 CD68及CD22阳性细胞在T1DM早期即浸润胰岛,有可能通过抗原递呈等作用促进了T1DM的发生。实验组小鼠血清IL-12增高,IL-4减少,提示Th1/Th2细胞失衡,推测是引发T1DM的重要因素之一。

英文摘要：

To explore the expression changes of immune cells which infiltrated the islets, and cytokines changes followed by type 1 diabetes mellitus（T1DM） in mice, we observed the changes of CD68/CD22 positive cells in islets of T1 DM mice, and detected serum levels of interleukin-12（IL-12） and interleukin-4（IL-4）. Total of 104 male C57BL/6J mice were divided into normal control group（NCG）, saline control group（SCG） and experimental group（EG）. Diabetes model was established by multiple low dose streptozotocin（MLD-STZ） injection（40 mg/kg body weight for 5 days）. The pancreas tail and serum were collected on days 3, 7, 10, 14, 21 and 28. As compared with NCG and SCG, numerical density on area（NA） of CD68 positive cells maintained at a high level in EG; the NAof CD22 positive cells in EG increased since day 3, but reduced after 7 days. IL-12 in serum of T1 DM mice increased since day 7, but IL-4 decreased, as compared with NCG and SCG（P 〈 0.05）. These results indicated that CD68 and CD22 positive cells infiltrate islets at the early stage and promote the T1 DM perhaps by antigen presentation. And the serum level of IL-12 is increased, but IL-4 decreased in EG, suggesting Th1/Th2 imbalance is existed.