Gołabek Violetta, Woźniakowska-Gesicka Teresa
III Klinika Pediatrii, Instytut Centrum Zdrowia Matki Polki w Łodzi.
Przegl Epidemiol. 2010;64(4):485-9.
Many individuals infected with HBV become chronic carriers and they liver disease may progress to cirrhosis and HCC. The newest data suggests that the interaction between positive and negative costimulatory molecules expressed on T cells are performing the role in the regulation ofT cells immune response. In the last years they were described programmed death-1 (PD-1) [CD279] and programmed death-ligand 1 (PD-L1) [CD274] in immunopathology of HBV infections. In acute exacerbation of hepatitis B, high level of PD-1 expression significantly mediated CD8+T cells apoptosis and protecting before damaging the liver. In the period of recovering, activation of the PD-1/PD-L 1 pathway should dynamically decrease, and if it isn't taking place, increased expression of the PD-1 plays a crucial role in inhibiting the function of virus-specific CD4+ and CD8+ T cells in chronic viral infections. The aim of this article was to explore the potential role of (PD-1/PD-L) pathway in antiviral immunity during HBV infection. Blockade of PD-1/PD-L1 pathway may open a novel therapeutic strategy for restoring the function of the exhausted CD8+ T cells, and enhancing viral control during chronic viral infections.
许多感染乙肝病毒（HBV）的个体成为慢性携带者，其肝脏疾病可能会发展为肝硬化和肝癌。最新数据表明，T细胞上表达的正负共刺激分子之间的相互作用在调节T细胞免疫反应中发挥作用。在过去几年中，程序性死亡1（PD-1）[CD279]和程序性死亡配体1（PD-L1）[CD274]在HBV感染的免疫病理学中被描述。在乙型肝炎急性加重期，高水平的PD-1表达显著介导CD8+T细胞凋亡，并在肝脏受损前起到保护作用。在恢复期间，PD-1/PD-L1途径的激活应动态降低，否则，PD-1表达增加在慢性病毒感染中抑制病毒特异性CD4+和CD8+T细胞功能方面起关键作用。本文旨在探讨（PD-1/PD-L）途径在HBV感染期间抗病毒免疫中的潜在作用。阻断PD-1/PD-L1途径可能为恢复耗竭的CD8+T细胞功能以及增强慢性病毒感染期间的病毒控制开辟一种新的治疗策略。
