关蛟 张正筠 周尊强 佟大年 周光文.Tfh 细胞在NOD小鼠糖尿病发病过程中的作用机制的研究[J].,2016,16(14):2604-2607 |
Tfh 细胞在NOD小鼠糖尿病发病过程中的作用机制的研究 |
The Role of Tfh in Diabetes of NOD Mice |
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DOI: |
中文关键词: Tfh 糖尿病 NOD |
英文关键词: Tfh Diabetes NOD |
基金项目:国家自然科学基金面上项目(81170721);上海市科委医学引导项目(14411960700);上海市科委浦江人才项目(14PJ1407300) |
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中文摘要: |
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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