Altered expression of SHIP, a Toll-like receptor pathway inhibitor, is associated with the severity of liver fibrosis in chronic hepatitis C virus infection.
作者： Antonios Katsounas , Martin Trippler , Shyam Kottilil , Richard A. Lempicki , Guido Gerken
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摘要: 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 microarray analysis in order identify gene expression patterns associated pathways PB fibrosis. Distinct regulation of inositol polyphosphate-5-phosphatase/145kDa (INPP5D or SHIP), a TLR2/TLR4-inhibitor, heat shock protein 8/22 kDa (HSPB8), an endogenous TLR4-ligand, during was identified could be confirmed by quantitative reverse-transcription polymerase chain reaction. These results suggest potential link activity the TLR4-pathway, SHIP-dependent regulation, liver
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