Editorial| Volume 68, ISSUE 4, P635-637, April 2018

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Interfering with Kupffer cell replenishment: New insights into liver injury

  • William Alazawi
    Corresponding author. Address: Barts Liver Centre, Blizard Insti, 4 Newark Street, London E1 2AT, United Kingdom. Tel.: +44 7882 7195.
    Barts Liver Centre, Blizard Institute, Queen Mary, University of London, London, United Kingdom
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  • Percy A. Knolle
    Institute of Molecular Immunology/Experimental Oncology, Klinikum rechts der Isar, Technische Universität München, München, Germany
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Published:February 17, 2018DOI:
      Interferon (IFN) has slipped off the hepatology radar in recent years, but a study by Borst and colleagues in this issue of Journal of Hepatology, reminds us that IFN signalling is an integral component of the liver’s highly coordinated response to viral infection and tissue injury.

      Linked Article

      • Type I interferon receptor signaling delays Kupffer cell replenishment during acute fulminant viral hepatitis
        Journal of HepatologyVol. 68Issue 4
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          Many different viral infections can cause acute hepatitis that may result in acute liver failure. Besides infections with hepatotropic virus (e.g., hepatitis B virus and hepatitis C virus) other viruses such as cytomegalovirus (CMV) can cause acute hepatitis.1–5 Yet, it is unclear to what extent viral pathogenicity or immunopathology cause liver damage. The liver is the central metabolic organ, which is characterized by a tolerogenic environment. Hepatic sinusoids are populated with antigen-presenting cells such as Kupffer cells (KC).
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