Abstract
Cells infected with the hepatitis B or C virus can be eliminated by an immune response mediated by cytotoxic T cells. Recently, the Fas Ligand has been detected on the surface of cytotoxic T cells, and is thought to induce cells to apoptosis by adhering to the Fas antigen. To evaluate the role of the Fas antigen and apoptosis in chronic hepatitis B or C, we used immunohistochemistry to study Fas antigen expression in liver samples obtained from 30 patients infected with chronic hepatitis B and 32 patients with chronic hepatitis C. In samples from patients with chronic hepatitis C and B, Fas antigen was mainly expressed in the cytoplasm (partly at the membrane) of hepatocytes, and these positive cells were detected especially at the periportal region near 'piecemeal necrosis'. According to Knodell's scoring system for the histological activity index, the scores of periportal inflammation and necrosis were higher in cases that were positive for Fas antigen than in cases that were negative for the antigen (n = 62, P < 0.001) and there was a positive correlation between these scores and the degree of Fas antigen expression (r = 0.621). There was also a positive correlation between the scores of intralobular inflammation and necrosis and the degree of Fas antigen expression (n = 62, r = 0.522, P = 0.001). Fas antigen was not detected in patients without hepatitis infection. These findings suggest that apoptosis of hepatocytes is induced via the Fas antigen and contributes to the elimination of infected cells.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.