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目的:观察聚乙二醇干扰素α-2a对慢性乙型肝炎患者外周血树突状细胞功能及B7-H1的影响,探讨慢性乙型肝炎病毒逃逸的的机制。方法:慢性乙型肝炎患者31例,给予聚乙二醇干扰素α-2a180μg抗病毒治疗52周,分别于0、12、26、52周检测肝功能、HBV-DNA;流式细胞术检测外周血mDC表面HLA-DR、CD80、CD86、CD83、CD1a、B7-H1水平。根据患者HBV-DNA水平,将患者分为应答组(A组)、非应答组(B组),10例健康志愿者作正常对照组(C组)。结果:慢性乙肝患者的树突状细胞膜表面分子HLA-DR、CD80、CD86、CD83、CD1a的表达均降低。聚乙二醇干扰素α-2a治疗后应答组膜表面分子HLA-DR、CD80、CD86、CD83、CD1a的表达高于非应答组65.3±6.2%vs 44.2±5.5%,67.2±7.4%vs 37.3±7.2%,68.4±3.6%vs 42.5±7.3%,65.6±6.8%vs 43.2±3.9%,49.4±9.5%vs 37.5±7.9%,(P<0.05)。应答组B7-H1表达水平较治疗前下降,非应答组B7-H1水平无明显变化12.73±3.8%vs 25.24±2.92%,(P<0.05)。结论:慢性乙型肝炎患者树突状细胞功能低下,聚乙二醇干扰素α-2a治疗可以提高树突状细胞功能,降低B7-H1表达,促进HBV-DNA的清除。树突状细胞功能低下及B7-H1高表达是乙型肝炎病毒免疫逃逸的因素之一。
Objective: To observe the effect of pegylated interferon α-2a on peripheral blood dendritic cell function and B7-H1 in patients with chronic hepatitis B and to explore the mechanism of escape of chronic hepatitis B virus. Methods: Thirty-one patients with chronic hepatitis B were treated with pegylated interferon alfa-2a 180μg antiviral therapy for 52 weeks. Liver function and HBV-DNA were detected at 0, 12, 26 and 52 weeks respectively. Flow cytometry Blood mDC surface HLA-DR, CD80, CD86, CD83, CD1a, B7-H1 levels. According to the level of HBV-DNA in patients, patients were divided into response group (group A), non-response group (group B) and 10 healthy volunteers as control group (group C). Results: The expression of HLA-DR, CD80, CD86, CD83 and CD1a on the surface of dendritic cells in patients with chronic hepatitis B were decreased. The expression of HLA-DR, CD80, CD86, CD83 and CD1a on the membrane surface of peginterferon alfa-2a group was higher than that of non-responder group (65.3 ± 6.2% vs 44.2 ± 5.5%, 67.2 ± 7.4% vs 37.3 ± 7.2%, 68.4 ± 3.6% vs 42.5 ± 7.3%, 65.6 ± 6.8% vs 43.2 ± 3.9%, 49.4 ± 9.5% vs 37.5 ± 7.9%, respectively (P <0.05). The expression level of B7-H1 in response group decreased compared with that before treatment, while the level of B7-H1 in non-response group had no significant change 12.73 ± 3.8% vs 25.24 ± 2.92% (P <0.05). Conclusion: The dendritic cells in patients with chronic hepatitis B have poor function. Peginterferon alfa-2a treatment can improve the function of dendritic cells, decrease the expression of B7-H1 and promote the clearance of HBV-DNA. Dendritic cell dysfunction and high expression of B7-H1 is one of the factors of hepatitis B virus immune escape.