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目的:观察乙型肝炎e抗原(HBeAg)对健康人单核细胞来源的树突状细胞(Dendritic cells,DCs)表面Toll样受体2(TLR 2)和程序性死亡配体-1(PD-L1)表达的影响,进一步探讨乙肝病毒感染慢性化过程中HBeAg的作用机制。方法:利用Ficoll分离法分离健康人外周血单个核细胞,经重组人粒细胞-巨噬细胞集落刺激因子(rhGM-CSF)、重组人白细胞介素4(rhIL-4)诱导培养树突状细胞,将第7天的细胞分成三组,分别为HBeAg刺激组、OVA无关蛋白对照组和未刺激组,经流式细胞仪检测CD11c+细胞表面TLR 2以及PD-L1的表达水平。结果:健康人单核细胞来源的树突状细胞经过HBeAg刺激9 h后,CD11c+细胞表面TLR 2的表达水平较未刺激组以及OVA无关蛋白对照组明显下降(P<0.01),同时可见CD11c+细胞表面PD-L1表达水平显著增加(P<0.01)。结论:HBeAg可以下调DCs表面TLR 2受体的表达,并上调其表面负性调节因子PD-L1的表达。HBV可通过HBeAg作用于抗原递呈细胞相关表面受体,从而影响了其正常功能,并最终影响免疫系统对病毒的清除作用,导致乙肝病毒感染的慢性化。
OBJECTIVE: To observe the effects of hepatitis B e antigen (HBeAg) on the expression of Toll-like receptor 2 (TLR 2) and PD-1 on human monocyte-derived dendritic cells (DCs) L1) expression, to further explore the role of HBeAg in the process of chronic hepatitis B virus infection. Methods: Peripheral blood mononuclear cells were isolated from healthy volunteers by Ficoll method. Dendritic cells (DCs) were induced by recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) and recombinant human interleukin-4 The cells on day 7 were divided into three groups: HBeAg stimulation group, OVA unrelated protein control group and unstimulated group. The expression of TLR 2 and PD-L1 on CD11c + cells was detected by flow cytometry. Results: After stimulated with HBeAg for 9 h, the expression of TLR2 on CD11c + cells was significantly decreased (P <0.01), and the expression of CD11c + cells in CD11c + cells was significantly lower than that in non-stimulated group and OVA- The expression of PD-L1 on the surface was significantly increased (P <0.01). Conclusion: HBeAg can down-regulate the expression of TLR 2 receptor on DCs and up-regulate the expression of PD-L1. HBV can act on antigen-presenting cell-related surface receptors through HBeAg, thus affecting its normal function and ultimately affecting the clearance of the immune system by the virus, resulting in the chronicization of hepatitis B virus infection.