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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Amphiregulin promotes the immunosuppressive activity of intrahepatic CD4(+) regulatory T cells to impair CD8(+) T-cell immunity against hepatitis B virus infection
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Amphiregulin promotes the immunosuppressive activity of intrahepatic CD4(+) regulatory T cells to impair CD8(+) T-cell immunity against hepatitis B virus infection

机译：两性调节蛋白促进肝内CD4（+）调节性T细胞的免疫抑制活性，从而削弱CD8（+）T细胞抵抗乙型肝炎病毒感染的免疫力

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Hepatitis B virus (HBV) infection causes liver diseases and hepatocellular carcinoma. Immunotolerance in HBV-infected patients is one of the factors that incur failure of HBV clearance and persistent HBV amplification. However, the mechanisms underlying immunotolerance after HBV infection are yet to be thoroughly understood. Using a novel HBV mouse model, we found for the first time that epidermal growth factor receptor (EGFR) is up-regulated on intrahepatic regulatory T (Treg) cells in HBV-infected mouse livers. The EGFR-positive Treg cells are more immunosuppressive than EGFR-negative Treg cells, demonstrated by higher expression of immunosuppressive cytokines and robust inhibition of CD8(+) T-cell proliferation in vitro. Furthermore, EGFR-positive Treg cells potently restrain CD8(+) T-cell-mediated anti-viral activity, leading to higher HBV burden in hepatocytes. Amphiregulin, a cytokine of the EGF family, is significantly up-regulated in HBV-infected livers, but the cellular sources of amphiregulin are still elusive. Amphiregulin promotes the immunosuppressive activity of EGFR-positive Treg cells in vitro, so as to profoundly inhibit production of anti-viral components in CD8(+) T cells. Taken together, our discovery elucidated a novel mechanism contributing to immunotolerance and viral amplification after HBV infection. Our study may provide new clues for developing therapeutic strategies against HBV infection.
机译：乙型肝炎病毒（HBV）感染会导致肝脏疾病和肝细胞癌。 HBV感染患者的免疫耐受性是导致HBV清除失败和持续HBV扩增的因素之一。但是，HBV感染后免疫耐受的潜在机制尚待彻底了解。使用新颖的HBV小鼠模型，我们首次发现表皮生长因子受体（EGFR）在HBV感染的小鼠肝脏中的肝内调节性T（Treg）细胞上调。 EGFR阳性Treg细胞比EGFR阴性Treg细胞更具免疫抑制作用，表现为更高的免疫抑制细胞因子表达和体外对CD8（+）T细胞增殖的强烈抑制作用。此外，EGFR阳性Treg细胞有效抑制CD8（+）T细胞介导的抗病毒活性，从而导致肝细胞中更高的HBV负担。两性调节蛋白是EGF家族的一种细胞因子，在HBV感染的肝脏中显着上调，但两性调节蛋白的细胞来源仍然难以捉摸。双调蛋白在体外可促进EGFR阳性Treg细胞的免疫抑制活性，从而深刻抑制CD8（+）T细胞中抗病毒成分的产生。综上所述，我们的发现阐明了一种新的机制，可促进HBV感染后的免疫耐受和病毒扩增。我们的研究可能为开发针对HBV感染的治疗策略提供新的线索。

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