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dc.contributor.authorDwyer, Benjamin
dc.contributor.authorOlynyk, John
dc.contributor.authorRamm, G.
dc.contributor.authorTirnitz-Parker, Nina
dc.identifier.citationDwyer, 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

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.

dc.publisherFrontiers Research Foundation
dc.subjectliver progenitor cells
dc.subjecthepatic stellate cells
dc.titleTWEAK and LTß Signaling during Chronic Liver Disease
dc.typeJournal Article
dcterms.source.titleFrontiers in Immunology

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.

curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusOpen access

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