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目的:研究滤泡辅助性T细胞(Follicular Helper T cell,Tfh)在非肥胖性糖尿病小鼠(Non-obese Diabetic mice,NOD)发病过程中的作用机制。方法:实验动物NOD小鼠按血糖值分为胰岛炎组(血糖浓度≤9 mmol/L)及糖尿病组(血糖浓度≥20 mmol/L)。ELISA法检测各组中糖尿病自身抗体谷氨酸脱羧酶抗体(65-kda glutamate decarboxylase antibody,GAD65Ab)、抗胰岛素自身抗体(Insulin autoantibody,IAA)表达水平,Western blot检测B细胞型淋巴瘤6蛋白(B-cell lymphoma 6 protein,Bcl-6)及可诱导共刺激分子(Inducible costimulatory molecule,ICOS)表达,流式细胞仪检测各组外周血及脾脏Tfh细胞水平。结果:糖尿病组NOD鼠自身抗体GAD65Ab(1.21±0.23 nmol/L)、IAA(0.96±0.12 nmol/L)浓度较胰岛炎组(0.32±0.09 nmol/L,0.25±0.06 nmol/L)均有明显升高;糖尿病组NOD鼠Bcl-6及ICOS表达较胰岛炎组NOD鼠有明显升高,外周血和脾脏Tfh细胞水平糖尿病组NOD鼠(24.55%)较胰岛炎组NOD鼠(4.27%)升高明显。结论:NOD小鼠自发糖尿病与自身抗体浓度升高相关,Tfh细胞可能参与NOD鼠糖尿病发生及发展过程。
Objective: To investigate the mechanism of Follicular Helper T cell (Tfh) in the pathogenesis of Non-obese Diabetic Mice (NOD). Methods: NOD mice were divided into insulitis group (blood glucose concentration ≤9 mmol / L) and diabetic group (blood glucose concentration≥20 mmol / L) by blood glucose level. The expression of GAD65Ab and IAA were detected by ELISA in all groups. Western blot was used to detect the expression of B-cell lymphoma 6 protein Bcl-6, Bcl-6, and ICOS were detected by flow cytometry. Tfh cells in peripheral blood and spleen were detected by flow cytometry. Results: The concentrations of GAD65Ab (1.21 ± 0.23 nmol / L) and IAA (0.96 ± 0.12 nmol / L) in diabetic NOD mice were significantly higher than that in insulitis group (0.32 ± 0.09 nmol / L, 0.25 ± 0.06 nmol / L) (P <0.05). Compared with NOD mice in insulitis group, the expression of Bcl-6 and ICOS in diabetic NOD group was significantly higher than that in NOD mice (24.55%) in Tfh cell level diabetic group and diabetic insulitis group (4.27% High obvious. CONCLUSIONS: Spontaneous diabetes in NOD mice is associated with elevated concentrations of autoantibodies, and Tfh cells may be involved in the pathogenesis of diabetes in NOD mice.