Vallbracht A, Maier K, Stierhof Y D, Wiedmann K H, Flehmig B, Fleischer B
Department of Medical Virology, University of Tübingen, FRG.
J Infect Dis. 1989 Aug;160(2):209-17. doi: 10.1093/infdis/160.2.209.
An autologous in vitro model was developed to analyze the immunologic cause of liver tissue injury during hepatitis A virus (HAV) infection. Human T lymphocytes infiltrating the livers of two patients with acute HAV infection were isolated from liver biopsy cores, cloned, and expanded in vitro. Procedures using a cell culture system with HAV-infected autologous skin fibroblasts demonstrated that 42% and 53% of the liver-infiltrating CD8+ clones were HAV-specific and that they kill HAV-infected skin fibroblasts in a human leukocyte antigen-restricted manner. Data show virus-specific killing by liver-infiltrating T lymphocytes in man and support the hypothesis that liver cell injury in acute HAV infection is mediated by HAV-specific CD8+ T lymphocytes and is not caused by a cytopathic effect of the virus itself.
构建了一个自体体外模型，以分析甲型肝炎病毒（HAV）感染期间肝组织损伤的免疫原因。从肝活检组织芯中分离出两名急性HAV感染患者肝脏中的人T淋巴细胞，进行克隆并在体外扩增。使用感染HAV的自体皮肤成纤维细胞的细胞培养系统进行的实验表明，42%和53%的肝脏浸润性CD8+克隆具有HAV特异性，并且它们以人类白细胞抗原限制的方式杀死感染HAV的皮肤成纤维细胞。数据表明人类肝脏浸润性T淋巴细胞具有病毒特异性杀伤作用，并支持以下假设：急性HAV感染中的肝细胞损伤是由HAV特异性CD8+T淋巴细胞介导的，而非病毒本身的细胞病变效应所致。
