中华实验和临床病毒学杂志
中華實驗和臨床病毒學雜誌
중화실험화림상병독학잡지
CHINESE JOURNAL OF EXPERIMENTAL AND CLINICAL VIROLOGY
2008年
5期
333-335
,共3页
吴学杰%陈姬%朱曼华%洪源%钟璐%王贵强
吳學傑%陳姬%硃曼華%洪源%鐘璐%王貴彊
오학걸%진희%주만화%홍원%종로%왕귀강
细胞因子类%肝炎病毒%乙型%PD-L1%PD-L2
細胞因子類%肝炎病毒%乙型%PD-L1%PD-L2
세포인자류%간염병독%을형%PD-L1%PD-L2
Cytokinins%Hepatitis B virus%PD-L1%PD-L2
目的 研究HBV转染的肝细胞系(HepG2.2.15细胞)在细胞因子作用下能否上调PD-L表达.方法 应用肝细胞系(HepG2细胞和HepG2.2.15细胞)为模型,用IL-4、IFN-α、IFN-γ(终质量浓度均为10 ng/ml,刺激时间为12 h)作用于上述细胞系,采用RT-PCR技术检测细胞因子作用前后PD-L表达情况.结果 无论是否转染HBV,IFN-α和IFN-γ均能诱导肝细胞系(HepG2细胞和HepG2.2.15细胞)PD-L1表达;而IL-4不能诱导PD-L1表达,IL-4、IFN-α、IFN-γ均能诱导转染了HBV的HepG2.2.15细胞PD-L2表达,仅IFN-γ能诱导未转染HBV的HepG2细胞PD-L2表达.结论 IFN-α和IFN-γ有较强诱导肝细胞系(HepG2细胞和HepG2.2.15细胞)PD-L1表达上调的作用,HBV在细胞因子诱导HepG2.2.15细胞PD-L2表达中具有促进作用.
目的 研究HBV轉染的肝細胞繫(HepG2.2.15細胞)在細胞因子作用下能否上調PD-L錶達.方法 應用肝細胞繫(HepG2細胞和HepG2.2.15細胞)為模型,用IL-4、IFN-α、IFN-γ(終質量濃度均為10 ng/ml,刺激時間為12 h)作用于上述細胞繫,採用RT-PCR技術檢測細胞因子作用前後PD-L錶達情況.結果 無論是否轉染HBV,IFN-α和IFN-γ均能誘導肝細胞繫(HepG2細胞和HepG2.2.15細胞)PD-L1錶達;而IL-4不能誘導PD-L1錶達,IL-4、IFN-α、IFN-γ均能誘導轉染瞭HBV的HepG2.2.15細胞PD-L2錶達,僅IFN-γ能誘導未轉染HBV的HepG2細胞PD-L2錶達.結論 IFN-α和IFN-γ有較彊誘導肝細胞繫(HepG2細胞和HepG2.2.15細胞)PD-L1錶達上調的作用,HBV在細胞因子誘導HepG2.2.15細胞PD-L2錶達中具有促進作用.
목적 연구HBV전염적간세포계(HepG2.2.15세포)재세포인자작용하능부상조PD-L표체.방법 응용간세포계(HepG2세포화HepG2.2.15세포)위모형,용IL-4、IFN-α、IFN-γ(종질량농도균위10 ng/ml,자격시간위12 h)작용우상술세포계,채용RT-PCR기술검측세포인자작용전후PD-L표체정황.결과 무론시부전염HBV,IFN-α화IFN-γ균능유도간세포계(HepG2세포화HepG2.2.15세포)PD-L1표체;이IL-4불능유도PD-L1표체,IL-4、IFN-α、IFN-γ균능유도전염료HBV적HepG2.2.15세포PD-L2표체,부IFN-γ능유도미전염HBV적HepG2세포PD-L2표체.결론 IFN-α화IFN-γ유교강유도간세포계(HepG2세포화HepG2.2.15세포)PD-L1표체상조적작용,HBV재세포인자유도HepG2.2.15세포PD-L2표체중구유촉진작용.
Objective To investigate whether the PD-L expression in the liver cell lines transinfected with HBV(HepG2.2.15 cells) can be up-regulated after cytokines stimulating. Methods To apply the liver cell lines (HepG2 cells and HepG2.2.15 cells) as a model, the cells were stimulated with IL-4, IFN-α and IFN-γ (final concentration were 10 ng/ml, stimulated for 12 hours) and RT-PCR was carried out to determine the PD-L expression before and after cytokines stimulating. Results Whether or not transinfected with HBV, IFN-α and IFN-γ both can induce the liver cell lines (HepG2 cells and HepG2.2.15 cells) PD-L1 expression while IL-4 can not; IL-4, IFN-α, IFN-γ all can induce the PD-L2 expression in HepG2.2.15 cells which was transinfected with HBV, only IFN-γ can induce the PD-L2 expression in HepG2 cells which was not transinfected with HBV. Conclusion IFN-α, IFN-γ both can induce the PD-L1 expression in HepG2 cells and HepG2.2.15 cells, while it is easy for cytokines to induce the PD-L2 expression in HepG2.2.15 cells which was transinfeeted with HBV, this may provide a potential mechanism of the molecular basis for chronic HBV infection.
