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    TWEAK and LTß Signaling during Chronic Liver Disease

    200128_130521_Dwyer_Front_Immunol_2014.pdf (1.103Mb)
    Access Status
    Open access
    Authors
    Dwyer, Benjamin
    Olynyk, John
    Ramm, G.
    Tirnitz-Parker, Nina
    Date
    2014
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Dwyer, B. and Olynyk, J. and Ramm, G. and Tirnitz-Parker, N. 2014. TWEAK and LTß Signaling during Chronic Liver Disease. Frontiers in Immunology. Advance online publication. DOI:10.3389/fimmu.2014.00039
    Source Title
    Frontiers in Immunology
    DOI
    10.3389/fimmu.2014.00039
    ISSN
    1664-3224
    School
    School of Biomedical Sciences
    Remarks

    Copyright©2014 Dwyer, Olynyk, Ramm and Tirnitz-Parker. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    URI
    http://hdl.handle.net/20.500.11937/4702
    Collection
    • Curtin Research Publications
    Abstract

    Chronic liver diseases (CLD) such as hepatitis B and C virus infection, alcoholic liver disease, and non-alcoholic steatohepatitis are associated with hepatocellular necrosis, continual inflammation, and hepatic fibrosis. The induced microenvironment triggers the activation of liver-resident progenitor cells (LPCs) while hepatocyte replication is inhibited. In the early injury stages, LPCs regenerate the liver by proliferation, migration to sites of injury, and differentiation into functional biliary epithelial cells or hepatocytes. However, when this process becomes dysregulated, wound healing can progress to pathological fibrosis, cirrhosis, and eventually hepatocellular carcinoma. The other key mediators in the pathogenesis of progressive CLD are fibrosis-driving, activated hepatic stellate cells (HSCs) that usually proliferate in very close spatial association with LPCs. Recent studies from our group and others have suggested the potential for cytokine and chemokine cross-talk between LPCs and HSCs, which is mainly driven by the tumor necrosis factor (TNF) family members, TNF-like weak inducer of apoptosis (TWEAK) and lymphotoxin-β, potentially dictating the pathological outcomes of chronic liver injury.

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