Missale G, Brems J J, Takiff H, Pockros P J, Chisari F V
Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, California 92037.
Hepatology. 1993 Sep;18(3):491-6.
The proliferative response of peripheral blood lymphocytes to the HBcAg was compared with serological, molecular and immunohistochemical parameters of hepatitis B virus infection and with biochemical and histological parameters of liver disease in a patient who received a completely human leukocyte antigen class I-mismatched liver allograft for fulminant hepatitis. The proliferative response increased progressively after transplantation, as hepatitis B virus infection became reestablished in the hepatic allograft. Strikingly, the HBcAg-specific T cells suddenly disappeared from the peripheral blood immediately before the acute onset of a severe necroinflammatory liver disease in which more than 80% of the hepatocytes expressed HBcAg. These observations are compatible with the hypothesis that human leukocyte antigen class I-independent hepatitis B virus-specific T cells might play a previously unsuspected role in the pathogenesis of hepatitis B virus-induced liver disease.
在一名因暴发性肝炎接受完全人类白细胞抗原I类不匹配肝脏同种异体移植的患者中，将外周血淋巴细胞对乙肝核心抗原（HBcAg）的增殖反应与乙肝病毒感染的血清学、分子和免疫组化参数以及肝病的生化和组织学参数进行了比较。移植后，随着乙肝病毒感染在肝脏同种异体移植中重新建立，增殖反应逐渐增加。引人注目的是，在一种严重坏死性炎症性肝病急性发作前，外周血中HBcAg特异性T细胞突然消失，在这种肝病中，超过80%的肝细胞表达HBcAg。这些观察结果与以下假设相符，即不依赖人类白细胞抗原I类的乙肝病毒特异性T细胞可能在乙肝病毒诱导的肝病发病机制中发挥了先前未被怀疑的作用。
