Iannacone Matteo, Sitia Giovanni, Ruggeri Zaverio M, Guidotti Luca G
Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA.
J Hepatol. 2007 Apr;46(4):719-26. doi: 10.1016/j.jhep.2007.01.007. Epub 2007 Jan 29.
Hepatitis B virus (HBV) causes acute and chronic necroinflammatory liver diseases and hepatocellular carcinoma (HCC). HBV replicates noncytopathically in the hepatocyte, and most of the liver injury associated with this infection reflects the immune response. While the innate immune response may not contribute significantly to the pathogenesis of liver disease or viral clearance, the adaptive immune response, particularly the cytotoxic T lymphocyte (CTL) response, contributes to both. Recent observations also reveal that antigen-nonspecific inflammatory cells enhance CTL-induced liver pathology and, more surprisingly, that platelets facilitate the intrahepatic accumulation of CTLs, suggesting that the host response to HBV infection is a highly complex but coordinated process. The notion that platelets contribute to liver disease and viral clearance by promoting the recruitment of virus-specific CTLs into the liver is a new concept in viral pathogenesis, which may prove useful to implement treatments of chronic HBV infection in man.
乙型肝炎病毒（HBV）可引发急性和慢性坏死性炎症性肝病以及肝细胞癌（HCC）。HBV在肝细胞内进行非细胞病变性复制，与这种感染相关的大多数肝损伤反映的是免疫反应。虽然固有免疫反应可能对肝病发病机制或病毒清除作用不大，但适应性免疫反应，尤其是细胞毒性T淋巴细胞（CTL）反应，对二者均有作用。最近的观察还发现，抗原非特异性炎症细胞会增强CTL诱导的肝脏病理变化，更令人惊讶的是，血小板会促进CTL在肝内的积聚，这表明宿主对HBV感染的反应是一个高度复杂但协调的过程。血小板通过促进病毒特异性CTL向肝脏募集而对肝病和病毒清除产生影响，这一概念是病毒发病机制中的一个新概念，可能对实施人类慢性HBV感染的治疗有用。
