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目的 探索乙型肝炎病毒 (HBV)持续存在和复制对干扰素 γ受体 (IFN γR)、IFN γ/STAT 1信号及MHC Ⅰ诱导表达的影响。方法 采用流式细胞术、Western blot及半定量逆转录 聚合酶链反应 (RT PCR)等方法 ,检测HepG2 .2 .15与HepG2肝母细胞瘤细胞株及人正常细胞株LO2的IFN γR表达 ;同时检测细胞IFN γR1对IFN γ的结合能力。观测不同时间段的IFN γ/p STAT1信号活化及IFN γ/MHC Ⅰ诱导效应。结果 HepG2 .2 .15细胞膜结合型及全细胞内IFN γR1表达高于其母源性细胞HepG2及正常肝细胞株LO2细胞 ;HepG2 .2 .15 细胞IFN γR1mRNA量显著高于HepG2及LO2细胞 (t=9.35 ,P <0 .0 1) ;HepG2 .2 .15 细胞全细胞IFN γR2表达低于HepG2及LO2细胞 ;两株肿瘤细胞存在内源性 p STAT1条带 ;HepG2 .2 .15细胞IFN γ/p STAT1、IFN γ/MHC Ⅰ诱导效应较母源细胞低下。拉米夫定抑制HBVDNA后 ,可上调HepG2 .2 .15细胞的IFN γ/MHC Ⅰ表达。结论 HBV持续存在和复制可降低IFN γ/STAT1及IFN γ/MHC Ⅰ诱导表达的敏感性 ;并能上调IFN γR1表达、下调IFN γR2表达。
Objective To investigate the effects of persistence and replication of hepatitis B virus (HBV) on the expression of IFNγR, IFNγ / STAT1 and MHC Ⅰ. Methods IFNγR expression in HepG2.2.15 hepatocellular carcinoma cell line and human normal cell line LO2 was detected by flow cytometry, Western blot and semi-quantitative RT-PCR. At the same time, the binding ability of IFNγR1 to IFNγ was detected. IFNγ / p STAT1 signal activation and IFNγ / MHC Ⅰ induction effect were observed at different time points. Results The expression of IFNγR1 in HepG2.2.15 cells was higher than that in HepG2 cells and LO2 cells in normal liver cells. The amount of IFNγR1 mRNA in HepG2.2.15 cells was significantly higher than that in HepG2 and LO2 cells (t = 9.35, P <0.01). The expression of IFNγR2 in HepG2.2.15 cells was lower than that in HepG2 and LO2 cells. There were endogenous p STAT1 bands in both tumor cells and IFNγ in HepG2.2.15 cells / p STAT1, IFNγ / MHC Ⅰ induction effect than maternal cells lower. Lamivudine inhibits HBVDNA and up-regulates IFNγ / MHC Ⅰ expression in HepG2.2.15 cells. Conclusions HBV persistence and replication can reduce the sensitivity of IFNγ / STAT1 and IFNγ / MHC Ⅰ induced expression; and can upregulate IFNγR1 expression and downregulate IFNγR2 expression.