Vascular adhesion molecule expression in viral chronic hepatitis: evidence of neoangiogenesis in portal tracts.

BACKGROUND/AIMS: T cell-mediated immune reactions could be crucial for hepatocellular damage in viral chronic hepatitis. The aims of this study were to compare the expression of activation and cell adhesion molecules on peripheral blood and intrahepatic lymphocytes from chronic hepatitis C and to analyze the intrahepatic expression of vascular adhesion molecules in viral chronic hepatitis.

METHODS

Lymphocytes from patients with chronic hepatitis C were studied by flow cytometry. Intrahepatic expression of vascular adhesion molecules was assessed by immunohistochemistry.

RESULTS

Liver-derived T cells showed a high expression of activation and cell adhesion molecules. Interestingly, we observed that vascular cell adhesion molecule 1 was up-regulated on both sinusoidal endothelial and portal dendritic cells. A novel finding was the neoformation of microvessels in inflamed portal tracts. An enhanced expression of endoglin was located on sinusoidal endothelial cells and on portal tracts.

CONCLUSIONS

Activated cytotoxic T cells, which showed an up-regulated expression of cell adhesion molecules, composed the majority of intrahepatic lymphocytes in chronic hepatitis C. The expression of vascular cell adhesion molecule 1 on portal dendritic cells and the microvessels neoformation in portal tracts from viral chronic hepatitis could define the main pathway for the recruitment and priming of liver-infiltrating T cells.