MHV-3诱导小鼠暴发性肝炎模型中γδT细胞的抑制性受体表达

摘要

目的：通过分析在MHV-3诱导的小鼠暴发性肝炎模型中,小鼠感染病毒前后γδT细胞其抑制性受体NKG2A表达情况,以此探讨爆发性肝炎初期疾病急速恶化的机制。方法：建立MHV-3诱导小鼠暴发性肝炎模型,观察小鼠的死亡率；并检测在不同感染时间点0 h、12 h、24 h、48 h时对小鼠肝组织行伊红-苏木精染色(HE染色),观察肝脏病理学改变,ALT和AST水平。流式细胞学方法,标记γδT细胞,并标记其NKG2A的表达。结果：MHV-3诱导小鼠暴发性肝炎模型中,γδT表面所表达活化性受体NKG2A表达维持低水平。结论：小鼠爆发性肝炎初期,肝脏重要的天然免疫效应细胞γδT细胞细胞表面抑制性受体NKG2A维持低水平表达,提示机体负调控机制缺失,导致γδT细胞可抑制性低下,最终引起免疫失衡。%Objective:To analyze mice MHV-3-induced fulminant hepatitis model ,mice were infected with the virus before and afterγδT cells its inhibitory receptor NKG2A expression ,in order to investigate the mechanism of the rapid deterioration of fulminant hepatitis early disease . Method:MHV-3 in mice induced fulminant hepatitis model ,mice were observed mortality;detection in different time point of infection 0 h ,12h , 24h ,48h line of mouse liver tissue Yihong-hematoxylin staining( HE staining )to observe the changes in liver pathology ,ALT and AST levels . Flow cytometry method ,labeledγδT cells ,and marked NKG2A expression . Result:MHV-3 induced mouse model of fulminant hepatitis ,γδT surface expressed by activated receptor NKG2A expression remained low . Conclusion:Mice early fulminant hepatitis ,liver important cells of the innate immune effector cellsγδT cell surface inhibitory receptors NKG2A maintain low levels of expression ,subject to negative regulation mechanism of the body missing ,leadingγδT cells inhibit decrease,eventually causing the immune imbalance .