Why was STAT1 elevation delayed in the NK cells compared to the other PEC populations examined? Promoter sequences in the STAT1 gene specific for STAT1 complexes may act to enhance STAT1 induction whenever STAT1 is activated (26) . Thus, any cytokine signaling through STAT1 would be expected to induce elevated STAT1 levels. In addition to type 1 IFN receptors, receptors for IFN-␥ also activate STAT1 (10). The results presented here suggest that NK cells might first respond to type 1 IFN expo-sure with IFN-␥ because of their high STAT4 levels, but once IFN-␥ is induced, it acts back on the cells to induce STAT1. This would explain the delay in STAT1 induction in NK cells compared to other subsets. Alternatively or additionally, it might just take longer for type 1 IFN to induce STAT1 in populations with high STAT4 levels. The NK cells in both the spleen (9) and peritoneum (Fig. 5) consistently have lower levels of STAT1. Because the spleen is a secondary compartment of infection, most of the NK cells may be experiencing cytokines produced earlier at other sites and/or not be synchronized to make a detectable short burst of IFN-␥ in this compartment. In any case, it is remarkable that there is a window of opportunity for IFN-␥ production under the conditions in the peritoneum given the link between this response and shutting it off. The pathway suggests that there will be a very early source of NK cell IFN-␥ whenever type 1 IFNs are induced.