The c-kit loss-of-function mutation W/Wv conferred a phenotype similar, with regard to DC-mediated NK cell activation, to that found with Gleevec treatment. (A) Deficient KIT signaling enhanced the capacity of DCs to stimulate the cytotoxic activity of NK cells in vitro. The experimental setting was identical to that represented in Figure 4A, except that BM-DCs derived from WT WBB6F1 mice (WT) or from c-kit-deficient WBB6F1 mice (W/Wv) were cocultured with WT NK cells and NK cytotoxicity was assessed on YAC-1 cells (12). (B) Deficient KIT signaling stimulated the capacity of DCs to elicit IFN-γ secretion by NK cells in vitro. Instead of measuring the cytotoxic activity as in A, the accumulation of IFN-γ in culture supernatants was assessed. (C) The W/Wv mutation allowed FL-mediated NK cell activation in vivo. WT and^- W/Wv mutant mice were treated with FL in vivo (same doses, schedule, and statistical methods as in Figure 3). All experiments were performed 3 times with similar results. ^#P < 0.05, significantly different from PBS-treated animals (in W/Wv and WT animals); *P < 0.05, significantly different from FL-treated animals.