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The pathogenesis of hepatic fibrosis in chronic human hepatitis C virus (HCV) infection is not well understood; however, an association between inflammatory activity and fibrogenesis is likely. HCV infection initiates an immediate inflammatory response in the liver. Immune-mediated liver disease is thought to be initiated by the HCV specific liverinfiltrating T-cells and amplified by antigen-nonspecific cells. Destruction of infected hepatocytes occurs by HCVspecific CTL clones via Fas ligands, TNFalpha and/or perforin mechanisms. Of three main intrahepatic lymphocyte subsets, neither CD3+CD56+ natural T (NT) lymphocytes nor CD3-CD56+ natural killer (NK) lymphocyte populations correlate with any biochemical, viral or histological parameters of fibrosis. A highly significant linear correlation, however, exists between fibrosis activity (by Knodell score) and intrahepatic CD3+CD56- T-lymphocytes [4]. There has been great progress made in our understanding of the cellular mechanisms of hepatic fibrosis. The recognition that the hepatic stellate cell (HSC) formerly know as lipocyte, Ito, or fat-storing cell, played a central role in the fibrotic response was key to our understanding.