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Cutting Edge |
*
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037;
Fourth Department of Internal Medicine, Tokyo Medical University, Tokyo, Japan; and
Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697
We have previously reported that intrahepatic NK T cells
activated by 
-galactosylceramide inhibit hepatitis B virus
replication noncytopathically in the liver of transgenic mice. This
effect is mediated by antiviral cytokines directly produced by
activated NK T cells and/or by other cytokine-producing inflammatory
cells that are recruited into the liver. In this study, we demonstrated
that IFN-
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
recruitment of lymphomononuclear inflammatory cells. Recruitment of
these cells was not necessary for the antiviral activity, indicating
that direct activation of the intrahepatic resident NK T cell is
sufficient to control viral replication in this
model.
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