Cutting edge: Inhibition of hepatitis B virus replication by activated NK T cells does not require inflammatory cell recruitment to the liver

We have previously reported that intrahepatic NK T cells activated by alpha -galactosylceramide inhibit hepatitis B virus replication noncytopathicall y in the liver of transgenic mice. This effect is mediated by antiviral cyt okines directly produced by activated NK T cells and/or by other cytokine-p roducing inflammatory cells that are recruited into the liver. In this stud y, we demonstrated that IFN-gamma produced by activated NK T cells induced parenchymal and nonparenchymal cells of the liver to produce high levels of CXC chemokine ligands 9 and 10, which mediated the intrahepatic recruitmen t of lymphomononuclear inflammatory cells. Recruitment of these cells was n ot necessary for the antiviral activity, indicating that direct activation of the intrahepatic resident NK T cell is sufficient to control viral repli cation in this model.