NDLI: Toll-Like Receptor Signaling and Liver Fibrosis

Content Provider	PubMed Central
Author	Aoyama, Tomonori Paik, Yong-han Seki, Ekihiro
Copyright Year	2010
Abstract	Liver fibrosis occurs as a wound-healing scar response following acute and chronic liver inflammation including alcoholic liver disease, non-alcoholic steatohepatitis, hepatitis B and C, and autoimmune hepatitis. Myofibroblasts, mainly transdifferentiated from hepatic stellate cells, are pivotal cell types that produce fibrillar collagen. The activation of inflammatory cells, including Kupffer cells, is a crucial step for activating hepatic stellate cells. Toll-like receptors (TLRs) are pattern recognition receptors that sense pathogen-associated molecular patterns (PAMPs), which discriminate the products of microorganisms from the host. TLRs are expressed on Kupffer cells, endothelial cells, dendritic cells, biliary epithelial cells, hepatic stellate cells, and hepatocytes in the liver. TLR signaling induces potent innate immune responses in these cell types. The liver is constantly exposed to PAMPs, such as LPS and bacterial DNA through bacterial translocation because there is a unique anatomical link, the portal vein system between liver and intestine. Recent evidence demonstrates the role of TLRs in the activation of hepatic immune cells and stellate cells during liver fibrosis. Moreover, crosstalk between TLR4 signaling and TGF-β signaling in hepatic stellate cells has been reported. This paper highlights the role of TLR signaling in stellate cell activation and the progression of liver fibrosis.
Related Links	http://dx.doi.org/10.1155/2010/192543
Starting Page	192543
File Format	PDF
ISSN	16876121
e-ISSN	1687630X
Journal	Gastroenterology Research and Practice
Volume Number	2010
Language	English
Publisher	Hindawi Publishing Corporation
Publisher Date	2010-01-01
Access Restriction	Open
Rights Holder	Hindawi Publishing Corporation
Subject Keyword	Hepatology Gastroenterology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Hepatology Gastroenterology

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