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首页> 外文期刊>Journal of Hepatology: The Journal of the European Association for the Study of the Liver >Hepatitis C virus core protein impairs in vitro priming of specific T cell responses by dendritic cells and hepatocytes.
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Hepatitis C virus core protein impairs in vitro priming of specific T cell responses by dendritic cells and hepatocytes.

机译：丙型肝炎病毒核心蛋白损害树突状细胞和肝细胞对特定T细胞反应的体外引发作用。

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BACKGROUND/AIMS: Hepatitis C virus leads to chronic hepatitis in the majority of infected individuals. The mechanism of viral persistence is not completely understood. Hepatitis C virus core protein is produced within hepatocytes and is secreted during HCV infection. Our study characterizes the effects of core protein on T cell priming in mice. METHODS: We used a system of antigen-specific in vitro priming of CD4(+) and CD8(+) T cells by myeloid dendritic cells, hepatoma cells or primary hepatocytes. Core protein was either added to the cultures or expressed by antigen-presenting cells. RESULTS: Antigen-presenting cells treated with core protein showed reduced surface expression of major histocompatibility molecules. Myeloid dendritic cells showed also reduced expression of costimulatory molecules. CD4(+) and CD8(+) T cells primed by these cells showed defects in activation, proliferation, and cytokine production. Importantly, CD4(+) and also CD8(+) T cells primed in the presence of core protein showedan increase in interleukin-10 production resembling the phenotype of regulatory T cells. CONCLUSIONS: Hepatitis C virus core protein inhibits priming of antigen-specific CD4(+) and CD8(+) T cell responses by downregulation of major histocompatibility molecules and costimulatory molecules on antigen-presenting cells and induces development of IL-10-producing T cells.
机译：背景/目的：丙型肝炎病毒在大多数感染者中导致慢性肝炎。病毒持久性的机制尚不完全清楚。丙型肝炎病毒核心蛋白在肝细胞内产生，并在HCV感染期间分泌。我们的研究表征了核心蛋白对小鼠T细胞启动的影响。方法：我们使用了由髓样树突状细胞，肝癌细胞或原代肝细胞对CD4（+）和CD8（+）T细胞进行抗原特异性体外引发的系统。核心蛋白要么添加到培养物中，要么由抗原呈递细胞表达。结果：核心蛋白处理的抗原提呈细胞显示主要组织相容性分子的表面表达降低。骨髓树突状细胞还显示出共刺激分子的表达降低。由这些细胞引发的CD4（+）和CD8（+）T细胞在激活，增殖和细胞因子产生中表现出缺陷。重要的是，在核心蛋白存在下引发的CD4（+）和CD8（+）T细胞显示出白细胞介素10产量的增加，类似于调节性T细胞的表型。结论：丙型肝炎病毒核心蛋白通过下调抗原呈递细胞上的主要组织相容性分子和共刺激分子来抑制抗原特异性CD4（+）和CD8（+）T细胞反应的启动，并诱导产生IL-10的T细胞的发育。 。

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