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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。

英文摘要:

Objective:To research the function mechanism of Follicular Helper T cell (Tfh) in Non-obese Diabetic mice (NOD).Methods:The NOD mice were divided into two groups according to their blood glucose level (Glu): the insulitis group (Glu≤ 9 mmol/L) and the diabetic group (Glu≥ 20 mmol/L). ELISA was used to test the level of diabetes autoantibody 65-kda glutamate decarboxylase antibody (GAD65Ab) and Insulin autoantibody (IAA). B-cell lymphoma 6 protein (Bcl-6) and Inducible costimulatory molecule (ICOS) were tested by Western blot. Tfh cell count was tested by Fluorescence activated cell sorting (FACS).Results:The level of GAD65Ab and IAA were much higher in diabetic group than that in insulitis group; Bcl-6 and ICOS were higher expressed indiabetic group than that in insulitis group; Tfh cell count were much higher in diabetic group than that in insulitis group.Conclusion:The autoantibody contributed to the diabetes progression and Tfh cell may participate in the pathogenesis of diabetes in NOD mice.

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