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研究自发的1型糖尿病雌鼠模型(NOD)在自然状态下发生1型糖尿病过程中CD4+CD25+T细胞的动态变化,旨在初步探讨调节性T细胞参与1型糖尿病发病的可能机制。采用雌性NOD小鼠作动物模型,每2周尾静脉采血1次,采用三色流式细胞术测定NOD小鼠外周血中CD4+CD25+T细胞(CD3+CD4+CD25+)的百分率。在32周时,对比发生糖尿病和未发生糖尿病NOD小鼠不同脏器中的CD4+CD25+T细胞阳性率。HE法检测胰岛炎。结果显示:(1)自第6周起NOD小鼠CD4+CD25+T细胞百分率逐渐降低。发生糖尿病NOD小鼠CD4+CD25+T细胞比率低于未发病NOD小鼠对照组(外周血分别为0.94%±0.21%、1.62%±0.23%,P=0.01;脾脏2.09%±0.14%、2.77%±0.36%,P=0.019),提示糖尿病NOD小鼠外周血中存在异常比例的CD4+CD25+T细胞;(2)32周龄糖尿病NOD小鼠与未发病NOD小鼠的CD4+CD25+T细胞抑制功能减低,与阳性对照组有显著性差异;(3)HE染色结果示糖尿病NOD小鼠胰岛结构完全破坏,胰岛炎程度较未发病NOD小鼠严重。该结果提示NOD小鼠发生糖尿病时免疫功能紊乱与CD4+CD25+T细胞参与调节及T细胞亚群变化相关,糖尿病的发生受致病性T细胞和调节性T细胞的调节。
To study the dynamic changes of CD4 + CD25 + T cells in spontaneous type 1 diabetic rat models (NOD) during the development of type 1 diabetes mellitus, and to explore the possible mechanism of regulatory T cells involved in the pathogenesis of type 1 diabetes mellitus. Female NOD mice were used as animal models. Blood was collected from tail vein every two weeks. The percentage of CD4 + CD25 + T cells (CD3 + CD4 + CD25 +) in peripheral blood of NOD mice was determined by three-color flow cytometry. At week 32, the positive rates of CD4 + CD25 + T cells in different organs of diabetic and non-diabetic NOD mice were compared. Insulitis detected by HE method. The results showed that: (1) The percentage of CD4 + CD25 + T cells in NOD mice decreased gradually from the 6th week. The percentage of CD4 + CD25 + T cells in diabetic NOD mice was lower than that in non-infected NOD mice (peripheral blood were 0.94% ± 0.21%, 1.62% ± 0.23%, P = 0.01; spleen 2.09% ± 0.14%, 2.77 % ± 0.36%, P = 0.019), suggesting abnormal CD4 + CD25 + T cells in peripheral blood of diabetic NOD mice; (2) CD4 + CD25 + T cells in NOD mice of 32- (3) The results of HE staining showed that the islet structure of diabetic NOD mice was completely destroyed, and the degree of insulitis was more serious than that of non-infected NOD mice. The results suggest that immune dysfunction in NOD mice is associated with the involvement of CD4 + CD25 + T cells and T cell subsets in diabetes. The pathogenesis of diabetes is regulated by pathogenic T cells and regulatory T cells.