3d mice similarly demonstrated a defect in liver IFN-c production in response to MCMV infection. In WT mice, IFN-c reached maximal levels of 350061200 pg/g liver at 40 h before contracting by approximately half at 48 h post-infection. In contrast, at 40 h post-infection, 3d mice induced 5-fold less IFN-c than WT (Fig. 2D ). NK cells are an important early source of IFNc in the liver during MCMV infection [24, 25] , and accumulated at this site in both WT and 3d mice (Fig. 2E ). Using intracellular cytokine staining, results shown in Fig. 2F demonstrate a 7-fold reduction in the absolute numbers of NK1.1+ TCRb-liver cells expressing IFN-c in 3d mice at 40 h post-infection as compared to WT. There were also fewer IFN-c-expressing liver NK cells in 3d mice by proportion (0.8%60.3% and 1%60.4%) when compared to WT (6%62% and 4%60.4%) at 40 h and 48 h, respectively. Together, these results demonstrate that, in addition to an effect on systemic cytokine production, combined endosomal TLR signals can affect the expression of critical proinflammatory cytokines in the liver during MCMV infection.