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作 者:董加秀[1] 赵守松[1] 高继君[2] 焦贤春[2] 李柏青[3] 金齐力[3] 崔琢[1]
机构地区:[1]蚌埠医学院第一附属医院,安徽蚌埠233000 [2]蚌埠医学院第二附属医院,安徽蚌埠233000 [3]蚌埠医学院,安徽蚌埠233000
出 处:《临床肝胆病杂志》2009年第3期167-170,共4页Journal of Clinical Hepatology
基 金:安徽省教育厅自然科学研究项目(2006KJ105C)
摘 要:目的探讨慢性乙肝病毒感染者外周血树突状细胞(DCs)亚群【髓系DC(MDC)和浆细胞DC(PDC)】的变化与血清HBVDNA的关系。方法采集健康人和慢性乙肝病毒感染者外周静脉抗凝全血,利用荧光抗体标记和流式细胞仪检测外周血树突状细胞亚群(MDC的特异性标记为L ineage-HLA-DR+CD11 c+,PDC的特异性标记为L ineage-HLA-DR+CD123+);固相放免法定量检测血清乙型肝炎病毒标志。结果慢性乙肝病毒感染者外周血PDC相对平均百分率低于健康对照者,但缺少统计学意义,MDC相对数量在两者间没有差别;血清HBeAg阳性慢性乙型肝炎患者外周血PDC相对数量显著高(P<0.01)于HBeAg阴性患者和健康人(P<0.05),而在上述3组中MDC相对数量无差异(P=0.194)。结论HBV感染可导致患者的免疫功能改变,使机体产生免疫耐受或DC的凋亡;慢性乙型肝炎患者外周血PDC增加与HBeAg血清转换有关,提示PDC可能有抑制病毒的作用。Objective To investigate the influence of serum HBVDNA levels on the characterizathion of circulating dendritic cell subsets in patients with chronic hepatitis B infection. Methods The plasmacytoid DC ( DC2, Lineage - HLA - DR + CD123 + ) and non - IFN - alpha producingmyeloid DC (DC1, Lineage - HLA - DR + CD1 lc + ) in fresh peripheral blood from chronic hepatitis B infection without any anti - viral treatment and healthy donors were enumerated by using four -color flow cytometry. The serological markers of hepatitis B virus were evaluated by solid phase radio Ly (RIA). Results Percentage of PDC in patientswith chronic hepatitis B was numerically decreased and subsequently Produce less than that of nomal controls, but without statistical difference. Further, serum HBeAg positive patients with chronic hepatitis B exhibited a significant increase in percentage of circulating PDC, compared with HBeAg negative patients and health donors (P 〈0.01; P 〈0. 05, respectively). And there is no significant difference of MDC in peripheral blood be- tween chronic hepatitis B patients and nomal controls or among three groups above (P = 0. 194). Conclusion The results suggested that the HBV infection may cause patient's immunity function change and lead to the immune tolerance or apoptosis ;The percentage of peripheral PDC is associated with the HBeAg seroconversion and may plays a role on inhibition of HBV replication in patients with chronic hepatitis B.
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