AI Article Synopsis

  • The study investigates how immune responses and iron levels influence the progression of hepatitis C to chronic disease, focusing on liver biopsies from 28 patients.
  • Researchers analyze the presence of various immunological markers, finding that CD8+ T-cells are negatively correlated with liver fibrosis and cluster in specific regions, indicating active immune engagement.
  • The results suggest that hepatitis C virus genotype affects the expression of MHC-I in the liver, potentially impacting the effectiveness of antiviral therapy, particularly in patients with genotype 3a.

Article Abstract

Background/aims: Host factors that may influence progression of hepatitis C infection to chronic hepatitis include T-cell responses and iron accumulation. We evaluated the hepatic expression of immunological markers relevant for a cytotoxic response in relation to viral and HFE genotype.

Methods: Frozen liver biopsies were obtained at diagnosis from 28 HFE genotyped patients. Sections stained for CD8, MHC-I, beta(2)m, HFE and CD68 were analyzed blind by morphometry. Response to therapy was available in 12 cases.

Results: A negative correlation was found between the number of CD8(+) cells and fibrosis. CD8(+) cells localized as clusters in portal tracts and sinusoids and were seen interacting with MHC-I positive lining cells. MHC-I and beta(2)m were expressed mainly in the endothelial and Kupffer cells. HFE was expressed in most, but not all, round and dendritic CD68(+) cells. Patients with virus genotype 3a had higher hepatic MHC-I and HFE expression, and a better-sustained response to IFN therapy than other patients.

Conclusions: In chronic hepatitis C virus infection MHC-I expression in the liver seems to relate to viral-genotype. In addition, the expression of MHC-I molecules by Kupffer cells places them as probable important players in the host response to HCV.

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Source
http://dx.doi.org/10.1016/j.jhep.2004.04.027DOI Listing

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