慢性乙型肝炎病毒感染对外周血单个核细胞中凋亡分子表达的影响及其与免疫功能的相关性

目的 研究慢性乙型肝炎病毒(HBV)感染对外周血单个核细胞中凋亡分子表达的影响及其与免疫功能的相关性.方法 选择76例慢性乙型肝炎(CHB)患者和体检的54例健康志愿者,分别作为CHB组和对照组,采集血清并测定凋亡分子含量、采集外周血单个核细胞并测定凋亡分子表达量以及免疫细胞含量.结果 CHB组患者血清中凋亡分子Fas、FasL、Caspase-3、Caspase-6、Caspase-8的含量以及外周血单个核细胞中Fas、FasL、Caspase-3、Caspase-6、Caspase-8的mRNA含量均显著高于对照组;CHB组患者外周血中CD3+ CD4+T细胞、CD3+ CD8+T细胞、CD16+ CD56+ NK细胞的百分比及CD4+/CD8+的比例均显著低于对照组;外周血单个核细胞中Fas、FasL、Caspase-3、Caspase-6、Caspase-8的mRNA含量与CD3+ CD4+T细胞、CD3 +CD8+T细胞、CD16+ CD56+自然杀伤(NK)细胞的百分比呈负相关.结论 慢性HBV感染能够增加外周血单个核细胞中凋亡分子的表达,进而造成T淋巴细胞和NK细胞凋亡、抑制细胞免疫应答和非特异性免疫应.

Effect of chronic HBV infection on the expression of apoptosis molecules in peripheral blood mononuclear cells and its correlation with immune function

Objective To study the effect of chronic HBV infection on the expression of apoptosis molecules in peripheral blood mononuclear cells and its correlation with immune function.Methods 76 cases of chronic hepatitis B (CHB) patients and 54 healthy volunteers were separately enrolled in CHB group and control group.Serum was collected and apoptosismolecules contents were determined,peripheral blood mononuclear cells were collected and apoptosismolecules expression and immune cells contents were determined.Results Fas,FasL,Caspase-3,Caspase-6,Caspase-8 contents in serum and Fas,FasL,Caspase-3,Caspase-6,Caspase-8 mRNA contents in peripheral blood mononuclear cells of CHB group were significantly higher than control group;percentage of CD3 + CD4 + T cells,CD3 + CD8 + T cells,CD16 + CD56 + NK cells in the peripheral blood and ratio of CD4 +/CD8 + of CHB group were significantly lower than control group;Fas,FasL,Caspase-3,Caspase-6,Caspase-8 mRNA contents in peripheral blood mononuclear cells were negatively correlated with percentage of CD3 + CD4 + T cells,CD3 + CD8 + T cells,CD16 + CD56 + NK cells.Conclusions Chronic HBV infection can increase the expression of apoptotic molecules in peripheral blood mononuclear cells,and then cause the apoptosis of T lymphocytes and NK cells,the inhibition of cellular immune response and non-specific immune response.