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慢性乙型肝炎肝内淋巴细胞浸润的免疫组织化学研究,特别强调淋巴细胞的活化状态。

Immunohistochemical studies on intrahepatic lymphocyte infiltrates in chronic type B hepatitis, with special emphasis on the activation status of the lymphocytes.

作者信息

Yang P M, Su I J, Lai M Y, Huang G T, Hsu H C, Chen D S, Sung J L

机构信息

Department of Internal Medicine, National Taiwan University, College of Medicine, Taipei, Republic of China.

出版信息

Am J Gastroenterol. 1988 Sep;83(9):948-53.

PMID:3137808
Abstract

To study the immunopathogenesis of chronic type B hepatitis, we used a panel of monoclonal antibodies to characterize the intrahepatic mononuclear cell infiltrates in 39 patients with various forms of chronic hepatitis induced by hepatitis B virus (HBV) and, for comparison, in 10 with non-A, non-B (NANB)-induced chronic hepatitis. In portal areas, the OKT4:OKT8 ratio reversed because of the relative increase of OKT8+ cells. The mean intraportal T4:T8 ratio was significantly lower in HBV-associated chronic active hepatitis (CAH) than in chronic persistent hepatitis induced by HBV or NANB viruses. OKT8+ cells were predominant in the infiltrates of periportal areas (piecemeal necrosis) and lobules. As to the activation status of the infiltrates, T10 was found much more frequently on mononuclear infiltrates of piecemeal necrosis and peripheral portion of portal areas in CAH cases, regardless of viral etiology, and its existence was correlated with the severity of CAH. Natural killer cells, killer cells, and B-cells played little role in the pathogenesis of hepatocytolysis. We conclude that T-cell cytotoxicity is the main mechanism of hepatocytolysis, either in lobules or in periportal regions, and that T10 antigen defines a group of cells which may play an important role associated with the formation of piecemeal necrosis.

摘要

为研究慢性乙型肝炎的免疫发病机制,我们使用一组单克隆抗体对39例由乙型肝炎病毒(HBV)引起的各种形式慢性肝炎患者以及10例由非甲非乙型(NANB)肝炎病毒引起的慢性肝炎患者(作为对照)的肝内单核细胞浸润情况进行了特征分析。在门管区,由于OKT8+细胞相对增多,OKT4:OKT8比例发生逆转。与由HBV或NANB病毒引起的慢性持续性肝炎相比,HBV相关性慢性活动性肝炎(CAH)患者的平均门管区内T4:T8比例显著降低。OKT8+细胞在汇管区周围(桥接坏死)和小叶浸润中占主导地位。至于浸润细胞的激活状态,无论病毒病因如何,在CAH病例中,T10在桥接坏死和门管区周边部分的单核浸润细胞中更为常见,且其存在与CAH的严重程度相关。自然杀伤细胞、杀伤细胞和B细胞在肝细胞溶解的发病机制中作用不大。我们得出结论,T细胞细胞毒性是小叶或汇管区周围肝细胞溶解的主要机制,并且T10抗原定义了一组可能与桥接坏死形成相关的重要细胞。

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