摘要
目的:检测在口腔扁平苔藓中异常活化的胰岛素样生长因子1-磷脂酰肌醇3激酶/哺乳动物雷帕霉素靶蛋白(insulin-like growth factor 1-phosphatidylinositol-3-kinase/the mammalian target of rapamycin,IGF1-PI3K/mTOR)信号通路对T细胞与角质形成细胞共培养环境中炎性细胞因子的影响。方法:通过外源性IGF1、LY294002、雷帕霉素评估IGF-PI3K/mTOR信号通路在活化T细胞中的作用,构建T细胞与角质形成细胞共培养模型,运用酶联免疫吸附试验(enzyme-linked immunosorbnent assay,ELISA)法检测细胞培养上清中白细胞介素-2(interleukin-2,IL-2)和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)分泌情况。结果:与单独培养的T细胞比较,T细胞与角质形成细胞共培养能促进TNF-α的分泌(P<0.05),而对IL-2的分泌无明显影响;而IGF1-PI3K/mTOR通路可减少共培养环境中IL-2和TNF-α水平(P<0.05)。结论:IGF1-PI3K/mTOR信号通路可调控T细胞与角质形成细胞共培养模型中炎性细胞因子的分泌,可能参与了口腔扁平苔藓免疫炎症的发生发展。
Objective:To investigate the influence of IGF1-PI3K/MTOR signaling pathway,which was abnormally activated in OLP,on the inflammatory cytokines in the interaction of T cells and keratinocytes in oral lichen planus(OLP).Methods:A transwell co-culture system composed of T cells and oral keratinocytes was used as a model of OLP in vitro.The effects of activated T cells pretreated with LY294002,rapamycin,and IGF1 on the levels of IL-2 and TNF-αin supernatant from T cell alone and co-culture system were detected via ELISA,respectively.Results:Compared to the T cells cultured alone,the interaction of keratinocytes and T cells could increase the secretion of TNF-α(P<0.05),but has no impact on the level of IL-2.Whereas the aberrant IGF1-PI3K/MTOR signaling decreased the IL-2 and TNF-αsecretion in the co-culture system(P<0.05).Conclusion:The IGF1-PI3K/MTOR signaling may modulate the cytokine networks in the crosstalk between T cells and keratinocytes and participate in the progression of OLP.
作者
马瑞洁
谭雅芹
周刚
MA Rui-jie;TAN Ya-qin;ZHOU Gang(Department of Oral Medicine,School and Hospital of Stomatology,Wuhan University,Wuhan 430079,China)
出处
《口腔医学研究》
CAS
北大核心
2019年第4期397-400,共4页
Journal of Oral Science Research
基金
国家自然科学基金(编号:81771080
81371147)
