Altered expression of SHIP, a Toll-like receptor pathway inhibitor, is associated with the severity of liver fibrosis in chronic hepatitis C virus infection.
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- Record sourced from PubMed, PMID 21917890.
- Also identified by DOI 10.1093/infdis/jir500 and PMC identifier 3173502.
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Abstract
Hepatitis C-related fibrogenesis has been shown to involve complex interactions between peripheral and hepatic immune responses. Peripheral whole blood (PB) samples from patients with chronic hepatitis C (n = 36) were subjected to microarray analysis in order to identify gene expression patterns associated with immune pathways in PB and hepatic fibrosis. Distinct regulation of gene expression of inositol polyphosphate-5-phosphatase/145kDa (INPP5D or SHIP), a TLR2/TLR4-inhibitor, and heat shock protein 8/22 kDa (HSPB8), an endogenous TLR4-ligand, during fibrogenesis was identified and could be confirmed by quantitative reverse-transcription polymerase chain reaction. These results suggest a potential link between peripheral activity of the TLR4-pathway, peripheral SHIP-dependent immune regulation, and liver fibrosis.
Medical subject headings
- Heat-Shock Proteins
- Hepacivirus
- Hepatitis C, Chronic
- Liver Cirrhosis
- Phosphoric Monoester Hydrolases
- Protein Serine-Threonine Kinases