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HBV感染患者2′,5′寡腺苷酸合成酶、IL-2和IL-12水平检测及意义
The levels of 2’,5’ oligoadenylate synthetase,interleukin 2 and interleukin 12 in hepatitis B virus infection
【摘要】 目的:选用2′,5′寡腺苷酸合成酶(2-5OAS)作为干扰素观察指标,IL-2、IL-12作为Th1应答观察指标,了解内源性干扰素系统和Th1应答在HBV感染发病机制中作用。方法:用放射同位素法测定单核细胞2-5OAS活性;ELISA法测定血清IL-2、IL-12。结果:无症状HBsAg携带组2-5OAS、IL-2、IL-12含量与正常对照组无显著差异(P>0.05),急性肝炎组均显著高于正常对照组(P<0.01),慢性乙型肝炎轻、中、重度组、慢性重型肝炎组、肝硬化组、肝癌组均显著低于正常对照组(P<0.05),并且随慢性肝炎病情加重以及肝硬化、肝癌发生而递减,其中肝硬化、肝癌组处于最低水平(与慢性肝炎各组比较P<0.05)。结论:在HBV感染发病过程的不同阶段和不同临床分型患者中,其内源性干扰素系统和Th1应答反应都是有显著差异的,细胞免疫对病毒感染的痊愈起主导作用。
【Abstract】 AIM:In order to study the effect of endogenous interferon system and Th1 response modes on hepatitis B virus infection,the 2’,5’ oligoadenylate synthetase(2-5OAS),IL-2 and IL-12 were selected as the research parameters.METHODS:The activity of 2-5OAS in peripheral blood mononeuclear cells was determined by sensitive radioenzymatic assay.IL-2 and IL-12 were determined by ELISA.RESULTS:Compared to normal control,the 2-5OAS,IL-2 or IL-12 were not significantly changed(P>0.05)in the asymptomatic HBsAg carricer group.The 2-5OAS,IL-2 and IL-12 were significantly up-regulated(P<0.01)in the group of acute hepatitis,but in the groups of chronic hepatitis,liver cirrhosis and hepatocellular carcinoma,the 2-5OAS,IL-2,IL-12 were significantly down-regulated(P<0.05).Moreover,with the progression of patient’s conditions and with the complications of liver cirrhosis and hepatocellular carcinoma,the 2-5OAS,IL-2 and IL-12 decreased progressively,the 2-5OAS,IL-2,IL-12 were the lowest in guoups of liver cirrhosis and hepatocellular carcinoma(vs each groups of chronic hepatitis,P<0.05).CONCLUSION:The endogenous interferon system and Th1 response are significantly alterable in the different period of hepatitis B virus infection and among the different clinical types.The cellular immunity plays an important role in recovery from HBV infection.
【Key words】 Hepatitis B virus; 2’,5’-oligoadenylate synthetase; Interleukin-2; Interleukin-12;
- 【文献出处】 中国病理生理杂志 ,Chinese Journal of Pathophysiology , 编辑部邮箱 ,2007年01期
- 【分类号】R512.62
- 【被引频次】8
- 【下载频次】127