[Tissue expression of antigenic recognition and intercellular adhesion molecules in chronic viral hepatitis].

OBJECTIVE

To analyze the expression of different HLA class I antigens and cell adhesion molecules on frozen liver sections from patients with chronic active hepatitis, types B and C.

EXPERIMENTAL

DESIGN

Liver biopsy samples were divided into two parts, one for routine histological examination and another, after snap-freezing and storing at -80 degrees C, for immunohistochemical analysis. To carry out immunoperoxidase and immunofluorescence stainings, a panel of monoclonal antibodies specific for HLA class I light (beta 2-microglobulin) and heavy chain determinants, and for adhesion molecules such as intercellular adhesion molecule-1 and lymphocyte function associate antigen-3 was used.

PATIENTS: Immunohistochemistry was performed in frozen liver biopsy sections from 25 patients with viral chronic active hepatitis, 10 type B and 15 type C. As controls, normal liver samples and liver specimens from patients with cholestasis or steatosis were also studied.

RESULTS

HLA class I light and heavy chain determinants were expressed on hepatocytes, biliary duct epithelium, sinusoidal lining cells and lymphocytes from patients and controls; however, the beta 2-microglobulin conformational epitope was undetectable on hepatocytes from normal livers or with cholestasis or steatosis, but clearly positive on hepatocytes from patients with hepatitis. In addition, in liver sections from controls no adhesion molecules positivity was detected on hepatocytes; by contrast, hepatocytes from patients with hepatitis showed markedly enhanced membranous reactivity for both adhesion molecules in areas of piecemeal and lobular necrosis.

CONCLUSIONS

Virus B and C infections could induce an increased hepatocellular expression of HLA-class I determinants, including the conformational epitope adequate for antigen presentation, and cell-cell adhesion molecules. These findings underline the role of cell mediated immune reactions in the pathogenesis of hepatic injury in viral chronic hepatitis.