Kupffer cell-derived FasL production was significantly attenuated both in-vivo and in-vitro. Similar to other immune cells, FasL receptor (Fas) was upregulated within Kupffer cells suggesting that FasL may auto-regulate its production by inducing its originator-cell death. The ability to manipulate interactions between Kupffer cells and hepatocytes may have important therapeutic implications. Interference of Hepatitis B Virus Gene Expression andReplication by siRNA.