Chronic hepatitis B and hepatocarcinogenesis: Does prevention of “collateral damage” bring the cure?

✍ Scribed by Tobias Manigold; Barbara Rehermann

• Book ID: 102242576
• Publisher: John Wiley and Sons
• Year: 2003
• Tongue: English
• Weight: 80 KB
• Volume: 37
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.510370328

✦ Synopsis

A persistent immune response to hepatitis viruses is a well-recognized risk factor for hepatocellular carcinoma. However, the molecular and cellular basis for the procarcinogenic potential of the immune response is not well defined. Here, using a unique animal model of chronic hepatitis that induces hepatocellular carcinogenesis, we demonstrate that neutralization of the activity of Fas ligand prevented hepatocyte apoptosis, proliferation, liver inflammation, and the eventual development of hepatocellular carcinoma. The results indicate that Fas ligand is involved not only in direct hepatocyte killing but also in the process of inflammation and hepatocellular carcinogenesis in chronic hepatitis. This is the first demonstration that amelioration of chronic inflammation by some treatment actually caused reduction of cancer development.

(2) Sitia G, Isogawa M, Kakimi K, Wieland SF, Chisari FV, Guidotti LG. Depletion of neutrophils blocks the recruitment of antigen-nonspecific cells into the liver without affecting the antiviral activity of hepatitis B virusspecific cytotoxic T lymphocytes.