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• W3040241190 abstract "Programmed death ligand 1 (PD-L1) has been recently shown to be a major obstacle to antiviral immunity by binding to its receptor programmed death 1 (PD-1) on specific IFN-γ producing T cells in chronic hepatitis B. Currently, IFN-α is widely used to treat hepatitis B virus (HBV) infection, but its antiviral effect vary greatly and the mechanism is not totally clear. We found that IFN-α/γ induced a marked increase of PD-L1 expression in hepatocytes. Signal and activators of transcription (Stat1) was then identified as a major transcription factor involved in IFN-α/γ-mediated PD-L1 elevation both in vitro and in mice. Blockage of the PD-L1/PD-1 interaction by a specific mAb greatly enhanced HBV-specific T cell activity by the gp96 adjuvanted therapeutic vaccine, and promoted HBV clearance in HBV transgenic mice. Our results demonstrate the IFN-α/γ-Stat1-PD-L1 axis plays an important role in mediating T cell hyporesponsiveness and inactivating liver-infiltrating T cells in the hepatic microenvironment. These data raise further potential interest in enhancing the anti-HBV efficacy of IFN-α and therapeutic vaccines." @default.
• W3040241190 created "2020-07-10" @default.
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• W3040241190 date "2020-07-06" @default.
• W3040241190 modified "2023-10-17" @default.
• W3040241190 title "PD-L1 upregulation by IFN-α/γ-mediated Stat1 suppresses anti-HBV T cell response" @default.
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• W3040241190 doi "https://doi.org/10.1371/journal.pone.0228302" @default.
• W3040241190 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7337294" @default.
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• W3040241190 hasPublicationYear "2020" @default.
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