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首页> 外文期刊>International immunopharmacology >Elevated interleukin-35 suppresses liver inflammation by regulation of T helper 17 cells in acute hepatitis B virus infection
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Elevated interleukin-35 suppresses liver inflammation by regulation of T helper 17 cells in acute hepatitis B virus infection

机译：升高的白细胞介素-35通过调节急性乙型肝炎病毒感染中的T辅助17细胞来抑制肝脏炎症

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摘要

Interleukin (IL)-35 is a responsive anti-inflammatory cytokine implicated in different diseases processes. It has been reported that elevated IL-35 contributed to immunosuppression in chronic hepatitis by modulation of T helper 17 (Th17) and regulatory T cells. However, the role of IL-35 in acute hepatitis B (AHB) was still not completely elucidated. Thus, in the present study, we analyzed the expression and regulatory activity of IL-35 to Th17 cells and inflammatory response during acute hepatitis B virus (HBV) infection in both peripheral blood cells isolated from AHB patients and in hydrodynamic induced HBV-infected mouse model. Plasma IL-35 level and circulating HBV peptides-induced Th17 frequency was significantly elevated in AHB patients, and IL-35 expression negatively correlated with liver inflammation. In vitro IL-35 stimulation to CD4(+) T cells purified from AHB patients down-regulated HBV peptides-induced Th17-phenotype, which presented as reduced IL-17 and IL-22 production. In vivo IL-35 administration dampened liver inflammation in HBV plasmid injected mice, however, did not affect HBV antigens production. This process was accompanied by suppression of natural killer cells and down-regulation of HBV peptides-induced Th17 cells in the liver, but did not affect total intrahepatic lymphocytes and other cell subsets numbers or chemokines expression in the liver. In conclusion, the current data indicated that IL-35 might be a novel mediator associated with hepatocytes damage and liver inflammation by regulating HBV peptides-induced Th17 cells during acute HBV infection. The potential anti-inflammatory property of IL-35 might be pivotal for developing new therapeutic approaches for hepatitis B.
机译：白细胞介素（IL）-35是一种敏感的抗炎细胞因子，其含有不同的疾病过程。据报道，通过调节T辅助17（TH17）和调节T细胞，升高的IL-35导致慢性肝炎免疫抑制。然而，IL-35在急性乙型肝炎（AHB）中的作用仍未完全阐明。因此，在本研究中，我们分析了从AHB患者和流体动力学诱导的HBV感染的小鼠中分离的外周血细胞中急性乙型肝炎病毒（HBV）感染期间IL-35至Th17细胞和炎症反应的表达和调节活动模型。在AHB患者中，血浆IL-35水平和循环HBV肽诱导的TH17频率显着升高，IL-35表达与肝脏炎症负相关。在体外IL-35刺激对CD4（+）T细胞的刺激，从AHB患者纯化的下调HBV肽诱导的TH17-表型，其作为减少的IL-17和IL-22产生。在体内IL-35给药中，HBV质粒注射小鼠中的湿润肝脏炎症并未影响HBV抗原产生。该方法伴随着抑制天然杀伤细胞和肝脏中HBV肽诱导的Th17细胞的下调，但不影响肝脏中总肝内淋巴细胞和其他细胞亚群数或趋化因子表达。总之，目前的数据表明，通过调节急性HBV感染期间通过调节HBV肽诱导的Th17细胞，IL-35可能是与肝细胞损伤和肝脏炎症相关的新介体。 IL-35的潜在抗炎性能可能是为开发乙型肝炎新治疗方法的关键态度。

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  • 来源
    《International immunopharmacology》 |2019年第2019期|共8页
  • 作者

    Teng Deng-Ke; Liu Yi; Lv Yi-Fei; Wang Li; Zhang Wei; Wang Jiu-Ping; Li Yu;

  • 作者单位

    Jilin Univ Dept Ultrasound China Japan Union Hosp Changchun 130033 Jilin Peoples R China;

    Xian Med Univ Dept Oncol Shaanxi Prov Peoples Hosp Xian 710068 Shaanxi Peoples R China;

    Xian Med Univ Affiliated Hosp 256 West Youyi Rd Xian 710068 Shaanxi Peoples R China;

    Xian Med Univ Affiliated Hosp 256 West Youyi Rd Xian 710068 Shaanxi Peoples R China;

    Fourth Mil Med Univ Xijing Hosp Dept Infect Dis 15 West Changle Rd Xian 710032 Shaanxi;

    Fourth Mil Med Univ Xijing Hosp Dept Infect Dis 15 West Changle Rd Xian 710032 Shaanxi;

    Xian Med Univ Affiliated Hosp 256 West Youyi Rd Xian 710068 Shaanxi Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 药理学;
  • 关键词

    Hepatitis B virus; Interleukin-35; T helper 17 cells; Liver inflammation; Acute infection;

    机译：乙型肝炎病毒;白细胞介素-35;T辅助17细胞;肝脏炎症;急性感染;

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