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丙型肝炎病毒感染的免疫发病机制。

The immunopathogenesis of hepatitis C virus infection.

作者信息

Nelson D R

机构信息

Section of Hepatobiliary Diseases, Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Florida, Gainesville, Florida, USA.

出版信息

Clin Liver Dis. 2001 Nov;5(4):931-53. doi: 10.1016/s1089-3261(05)70202-6.

DOI:10.1016/s1089-3261(05)70202-6
PMID:11685802
Abstract

The outcome of HCV infection is determined by the interaction between the virus and the host immune system. The persistence of infection in most HCV-infected individuals, despite the presence of HCV-directed antibodies, suggests that such antibodies fail to induce viral clearance. Patients with self-limited hepatitis C have evidence of a polyclonal, multispecific CD8+ T-cell response along with a coordinated CD4+ T-cell response that is associated with eradication of HCV infection. Cytokines are produced both locally within the liver and systemically and may play an important role in controlling viral replication and contributing to hepatocellular damage through amplification of a nonspecific immune response. In most patients, the humoral, cellular immune, and cytokine response seem insufficient to eradicate infection. In its attempt to clear the virus from the liver, the immune system contributes to the hepatocellular injury seem in most chronically infected patients. A better understanding of the host's immune response may provide further insight on the pathogenetic mechanisms involved in development of chronic hepatitis and aid the development of better therapeutic strategies.

摘要

丙型肝炎病毒(HCV)感染的结果取决于病毒与宿主免疫系统之间的相互作用。在大多数HCV感染个体中,尽管存在针对HCV的抗体,但感染仍持续存在,这表明此类抗体无法诱导病毒清除。自限性丙型肝炎患者有证据表明存在多克隆、多特异性CD8 + T细胞反应以及与之协调的CD4 + T细胞反应,这与HCV感染的根除有关。细胞因子在肝脏局部和全身均有产生,可能在控制病毒复制以及通过放大非特异性免疫反应导致肝细胞损伤方面发挥重要作用。在大多数患者中,体液免疫、细胞免疫和细胞因子反应似乎不足以根除感染。在试图从肝脏清除病毒的过程中,免疫系统导致了大多数慢性感染患者出现肝细胞损伤。更好地了解宿主的免疫反应可能会进一步深入了解慢性肝炎发生发展所涉及的发病机制,并有助于开发更好的治疗策略。

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