We observed significant reductions in the numbers of NK cells in the lung airways of influenza-infected animals in which IL-15 was blocked at time points associated with their arrival at the site of infection, and failure of these cell populations to accumulate had implications in early viral control (Figure 2) . In order to determine whether IL-15 might be an important signal for NK cells in the migration to and/or the proliferation within the site of infection, we chose to provide exogenous IL-15 in an attempt to enhance any IL-15-dependent NK cell migration and/or in situ proliferation within the lung airways of influenza-infected animals. To this end, either PBS or recombinant IL-15/IL-15Ra fusion protein complexes (IL-15c) were administered intranasally to mice three days following influenza infection. To ensure that any biological effects of the IL-15c could be attributed to activity of the cytokine (which is merely stabilized by complexing to IL-15Ra), a control group of mice received the IL-15Ra only. Concurrent with treatment, mice received an i.p. pulse of the thymidine analog BrdU to identify proliferating cells. Twelve hours post treatment, the frequency and total number of NK cells in the BAL was quantified as well as the percentage of these cells incorporating BrdU. Isolated cells were simultaneously stained with 7-AAD as an indicator of cell viability, as only cells with disrupted membranes stain positive for this fluorescent dye. Importantly, neither the IL-15Ra alone nor the IL-15c affected cell viability, as cells isolated from animals receiving these treatments had similar percentages of 7-AAD + NK cells as those from PBS-treated mice (data not shown).