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目的 分析乙型肝炎病毒 (HBV)感染引起的慢性肝炎和肝炎肝硬变患者体内树突状细胞 (DC)亚群 (包括MDC和PDC)的数量和功能变化。方法 采用流式细胞分析技术检测 12例急性乙型肝炎、4 3例慢性乙型肝炎、15例肝炎肝硬变患者及 2 2例健康人体内MDC和PDC细胞的比例和数量 ;体外培养患者及健康人外周血DC1并检测其表型和刺激混合淋巴细胞反应 (MLR)的能力 ,评价MDC的功能 ;用 1型单纯疱疹病毒 (HSV 1)刺激外周血单个核细胞 (PBMCs)并与PBMCs共培养 ,通过检测PBMCs产生的α 干扰素水平评估PDC的功能。结果 慢性乙型肝炎患者的DC1表面CD80、CD86的表达水平低于健康人 ;健康人外周血MDC的比例为 0 .4 5 %± 0 .14 % ,绝对数为 (11.3± 6 .3)× 10 6个 L ,两者在肝炎肝硬变患者下降 ;而健康人外周血PDC的比例为 0 .36 %± 0 .15 % ,绝对数为 (8.9±4 .2 )× 10 6 个 L ,两者在慢性肝炎和肝炎肝硬变患者均下降 ;慢性肝炎和肝硬变患者PDC分泌的α 干扰素量也低于健康人。结论 乙肝病毒感染慢性化后 ,患者体内两种DC均出现数量和功能异常 ,这种异常可能是导致HBV感染的慢性化和疾病进程的原因之一
Objective To analyze the quantitative and functional changes of dendritic cells (DCs) subsets (including MDC and PDC) in patients with chronic hepatitis and cirrhosis due to hepatitis B virus infection. Methods Flow Cytometry was used to detect the proportion and number of MDC and PDC cells in 12 patients with acute hepatitis B, 43 with chronic hepatitis B, 15 with cirrhosis and 22 healthy individuals. In vitro culture of patients and The peripheral blood mononuclear cells (PBMCs) were stimulated with herpes simplex virus type 1 (HSV 1) and their co-activity with PBMCs was evaluated by measuring their phenotype and the ability to stimulate mixed lymphocyte reaction (MLR) Cultures were evaluated for PDC function by measuring the level of interferon alpha produced by PBMCs. Results The expression of CD80 and CD86 on the surface of DC1 in patients with chronic hepatitis B was lower than that in healthy people. The percentage of MDC in peripheral blood was 0.45% ± 0.14% and the absolute number was (11.3 ± 6.3) × 10 6 L, both decreased in patients with hepatitis cirrhosis; while the proportion of healthy people in the peripheral blood PDC was 0.36% ± 0.15%, the absolute number was (8.9 ± 4 .2) × 10 6 L, Both declined in patients with chronic hepatitis and cirrhosis of the liver; the amount of interferon alpha secreted by the PDC in patients with chronic hepatitis and cirrhosis was also lower than in healthy people. Conclusions After chronic hepatitis B virus infection, both DCs appear abnormal in quantity and function in vivo. This abnormality may be one of the reasons leading to chronic HBV infection and progression of the disease