中文摘要：

目的探讨暴发性肝炎初期疾病急速恶化的机制，探讨在3型鼠肝炎病毒（MHV-3）诱导的小鼠爆发性肝炎模型中，小鼠感染病毒前后γδT细胞其活化受体NKG2D表达情况。方法建立MHV-3诱导小鼠暴发性肝炎模型，在不同感染时间点0、24、48h时对小鼠肝组织行苏木精-伊红染色（HE染色），观察肝脏病理学改变，并检测血清谷丙转氨酶（ALT）和谷草转氨酶（AST）水平。采用流式细胞学方法标记γδT细胞，并标记其NKG2D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NKG2D表达增高。结论小鼠暴发性肝炎初期，肝脏重要的天然免疫效应细胞γδT细胞表面活化性受体NKG2D表达增高。

英文摘要：

Objective To analyze γδT cell activating receptor NKG2D expression, in MHV-3 induced mice fulminant hepatitis model and to explore the rapid deterioration of fulminant hepatitis early disease. Methods MHV-3 in mice induced fulminant hepatitis. Hematoxylin and eosin stain （HE stain） of the liver, serum ALT and AST levels were observed. Flow cytometry was used to label γδT cells and mark NKG2D expression. Results In MHV-3 induced mouse model of fulminant hepatitis, γδT surface expressed activating receptor NKG2D expression was increased. Conclusion In mice acute fulminant hepatitis, innate immune effector cells γδT cells cell surface activating receptor NKG2D expression is increased.