文章摘要
宣世英,孙樱,张健,李清华,吕维红,姜岭梅,吴树华,邹波.慢性乙型肝炎病人外周血单个核细胞HBV感染后对其细胞免疫功能影响的研究[J].中华流行病学杂志,1997,18(2):80-82
慢性乙型肝炎病人外周血单个核细胞HBV感染后对其细胞免疫功能影响的研究
The Influence to the Function 0f Cellular Immunity after Being Infected by HBV in the PBMC in Chronic Hepatitis B
收稿日期:1996-08-28  出版日期:2021-06-09
DOI:
中文关键词: 慢性乙型肝炎  NK细胞活性  T细胞亚群比值  可溶性白细胞介素2受体  细胞免疫功能
英文关键词: Chronic hepatitis B  NK cells  Subgroup of T cells  sIL-2R  The function of cellular immunity
基金项目:
作者单位
宣世英 山东省青岛市市立医院 266011 
孙樱 山东省青岛市市立医院 266011 
张健 山东省青岛市市立医院 266011 
李清华 山东省青岛市市立医院 266011 
吕维红 山东省青岛市市立医院 266011 
姜岭梅 山东省青岛市市立医院 266011 
吴树华 山东省青岛市市立医院 266011 
邹波 山东省青岛市市立医院 266011 
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中文摘要:
      应用聚合酶链(PCR)方法检测慢性乙型肝炎(乙肝)病人外周血单个核细胞(PBMC)内乙肝病毒DNA (HBV DNA)。54例PBMC内HBV DNA (+)和71例PBMC内HBV DNA (-)病例平行测定自然杀伤细胞(NK)活性、T细胞亚群比值(CD4/CD8)和血清可溶性白细胞介素2受体(sIL-2R)。结果示慢性乙肝病人PBMC内HBV DNA (+)组NK、CD4/CD8和sIL-2R与正常对照组及PBMC内HBV DNA (-)组病人相比差异均有非常显著性(P<0.001)。同时发现慢性乙肝PBMC内HBV DNA (+)病人NK活性、CD4/CD8比值和sIL-2R水平有直线相关性(P均<0.01),而PBMC内HBV DNA (-)病人,仅CD4/CD8比值和sIL-2R水平呈相关性(P<0.001) NK活性尚未受到明显影响。结果表明,HBV感染PBMC导致慢性乙肝病人细胞免疫功能紊乱,有助于阐明慢性乙肝的发病机制,并有可能为乙肝的防治提供理论依据。
英文摘要:
      In this study, HBV DNA was detected by PCR from PBMC of chronic hepatitis B. A total number of 54 cases were positive and 71 cases were negative. When detecting the competence of NK cells, the subgroup of T cells the ratio of CD4/CD8, the concentration of sIL-2R in three groups, and between the two CHB groups and a normal control group, the differences between HBV DNA positive group and HBV DNA negative group and between HBVDNA positive group and the normal control group were all dramatically significant (P < 0.01). We also found that a lineal correlation of the competence of NK cells, the ratio of CD4/CD8 and the concentration of sIL-2R(P < O. 01) in the positive group,whereas in the negative group only the ratio of CD4/CD8 was consistent with the concentration of sIL-2R(P < 0.01), and the competence of NK cells did not decrease obviously. The results indicated that it was the infection of HBV in PBMC which caused the disorder of the function of cellular immunity. This finding helped us to explain the pathogenesis of hepatitis B. It could also lay a theoretical ground for the prevention and the treatment of hepatitis B.
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