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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >MicroRNA-155 regulates interferon-gamma production in natural killer cells via Tim-3 signalling in chronic hepatitis C virus infection
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MicroRNA-155 regulates interferon-gamma production in natural killer cells via Tim-3 signalling in chronic hepatitis C virus infection

机译：MicroRNA-155在慢性丙型肝炎病毒感染中通过Tim-3信号调节自然杀伤细胞中干扰素-γ的产生

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Host immune responses must be tightly regulated by an intricate balance between positive and negative signals while fighting pathogens; persistent pathogens may usurp these regulatory mechanisms to dampen host immunity to facilitate survival in vivo. Here we report that Tim-3, a negative signalling molecule expressed on monocytes and T cells, is up-regulated on natural killer (NK) cells in individuals chronically infected with hepatitis C virus (HCV). Additionally, the transcription factor T-bet was also found to be up-regulated and associated with Tim-3 expression in NK cells during chronic HCV infection. MicroRNA-155 (miR-155), an miRNA that inhibits signalling proteins involved in immune responses, was down-regulated in NK cells by HCV infection. This Tim-3/T-bet over-expression and miR-155 inhibition were recapitulated in vitro by incubating primary NK cells or NK92 cell line with Huh-7 hepatocytes expressing HCV. Reconstitution of miR-155 in NK cells from HCV-infected patients led to a decrease in T-bet/Tim-3 expression and an increase in interferon-gamma production. Blocking Tim-3 signalling also enhanced interferon-gamma production in NK cells by improving signal transducer and activator of transcription-5 phosphorylation. These data indicate that HCV-induced, miR-155-regulated Tim-3 expression regulates NK cell function, suggesting a novel mechanism for balancing immune clearance and immune injury during chronic viral infection.
机译：在抵抗病原体时，必须通过正负信号之间的复杂平衡来严格调节宿主的免疫反应。持久性病原体可能会篡改这些调节机制，从而减弱宿主免疫力，促进体内存活。在这里我们报告说，Tim-3，在单核细胞和T细胞上表达的阴性信号分子，在慢性感染丙型肝炎病毒（HCV）的个体的自然杀伤（NK）细胞上被上调。另外，在慢性HCV感染期间，还发现转录因子T-bet在NK细胞中被上调并与Tim-3表达相关。 MicroRNA-155（miR-155）是一种抑制参与免疫应答的信号蛋白的miRNA，在HCV感染的NK细胞中被下调。通过将原代NK细胞或NK92细胞系与表达HCV的Huh-7肝细胞一起孵育，可以在体外概括Tim-3 / T-bet过表达和miR-155抑制。 HCV感染患者的NK细胞中miR-155的重建导致T-bet / Tim-3表达的减少和干扰素-γ产生的增加。通过改善信号转导子和转录5磷酸化的活化剂，阻断Tim-3信号传导还可增强NK细胞中干扰素的产生。这些数据表明，HCV诱导的，miR-155调节的Tim-3表达调节NK细胞功能，提示在慢性病毒感染期间平衡免疫清除和免疫损伤的新机制。

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