摘要
目的:探讨内质网应激在T细胞活化诱导细胞凋亡(activation-induced cell death,AICD)中的作用。方法:建立小鼠T淋巴瘤EL-4细胞和成年C57BL/6小鼠T细胞AICD的模型,流式细胞术测定发生AICD的细胞凋亡率;流式细胞术测定不同浓度CD3抗体对EL-4细胞AICD发生的影响;将小鼠AICD模型T细胞分为对照组、模型组、激动组(加入内质网应激激动剂二硫苏糖醇)、抑制组(加入内质网应激抑制剂4-苯基丁酸),流式细胞术测定各组细胞凋亡率。结果:EL-4细胞和C57BL/6小鼠T细胞发生AICD时,细胞凋亡率升高;随着CD3抗体浓度增加,EL-4细胞发生AICD的比例增加;激动组小鼠T细胞发生AICD的比例增加,抑制组小鼠T细胞发生AICD的比例降低;抑制剂组细胞凋亡水平较对照组降低。结论:增强内质网应激可促进T细胞发生AICD,抑制内质网应激可减少T细胞发生AICD。
Objective:To explore the role of endoplasmic reticulum(ER) stress in activation-induced cell death(AICD) of T cells.Methods:The model of AICD was set up by using EL-4 cells(mice T lymphoma cell) and the T cell of adult C57BL/6 mice, the cell apoptosis of AICD was measured by flow cytometry.The effect of CD3 antibody concentrations on EL-4 cell AICD was assessed by flow cytometry.Flow cytometry was used to observe and analyze the apoptotic cells of agonist group which added with ER stress inducer dithiothreitol and inhibition group which added with ER stress inhibitor 4-phenylbutyric acid in T cell AICD of adult C57BL/6 mice.Results:The cell apoptosis was increased when AICD formed in EL-4 cell and T cell in C57BL/6 mice.With the increase of CD3 antibody concentration, the occurrence rate of EL-4 cell AICD increased.Dithiothreitol induced the occurrence of T cell AICD in mice, while 4-phenylbutyric acid reduced the occurrence of T cell AICD in mice.Conclusion:The induction of ER stress could promote T cell AICD, while inhibition of ER stress decrease T cell AICD.
出处
《江苏大学学报(医学版)》
CAS
2017年第3期205-208,共4页
Journal of Jiangsu University:Medicine Edition
基金
国家自然科学基金资助项目(81172834
31428006
31570879)
关键词
内质网应激
T细胞
活化诱导细胞凋亡
endoplasmic reticulum stress
T cell
activation-induced cell death