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TWEAK and LTβ signaling during chronic liver disease
Journal article   Open access   Peer reviewed

TWEAK and LTβ signaling during chronic liver disease

B.J. Dwyer, J.K. Olynyk, G.A. Ramm and J.E.E. Tirnitz-Parker
Frontiers in Immunology, Vol.5
2014
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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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Collaboration types
Domestic collaboration
Citation topics
1 Clinical & Life Sciences
1.102 Stem Cell Research
1.102.1150 Hepatocyte Growth Factor
Web Of Science research areas
Immunology
ESI research areas
Immunology
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