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Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037
In this study we evaluated the ability of activated intrahepatic
APCs to inhibit hepatitis B virus (HBV) replication in transgenic mice.
Intrahepatic APCs were activated by administration of an anti-CD40
agonistic mAb (
CD40). We showed that a single i.v. injection of
CD40 was sufficient to inhibit HBV replication noncytopathically by
a process associated with the recruitment of dendritic cells,
macrophages, T cells, and NK cells into the liver and the induction of
inflammatory cytokines. The antiviral effect depended on the production
of IL-12 and TNF- by activated APCs; however, it was mediated
primarily by IFN-
produced by NK cells, and possibly T cells, that
were activated by IL-12. Collectively, these results suggest that
activated APCs can directly produce antiviral cytokines (IL-12,
TNF-) and trigger the production of other cytokines (i.e., IFN-)
by other cells (e.g., NK cells and T cells) that do not express CD40.
These results provide insight into a hitherto unsuspected antiviral
function of intrahepatic APCs, and they suggest that therapeutic
activation of APCs may represent a new strategy for the treatment of
chronic HBV infection.
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