Type I IFNs expressed within hours after viral infection have been documented to induce expression of the chemokines CXCL9 and 10 which function to recruit CXCR3 expressing NK cells to sites of infection [15] . However, Type I IFNs also modulate the expression of the common gamma chain cytokine interleukin 15 [16, 17, 18] , which we recently reported to be temporally and locally increased following influenza infection [19] . This expression of IL-15 in the respiratory tract facilitates the recruitment of antigen-specific CD8 T cells to the respiratory tract. However, it is unclear whether the chemotactic properties of IL-15 uniquely affect migratory CD8 T cells or could be extended to other IL-15-sensitive immune cells. NK and NKT cells are nearly absent in IL-15 2/2 animals [20] , highlighting the important role of IL-15 on NK cell development and homeostasis in the steady-state. Following viral infections, de novo production of IL-15 by dendritic cells results in the activation and proliferation of NK cells [21, 22] , and transient systemic stimulation of NK cells with soluble IL-15/IL-15Ra complexes also results in an accumulation of phenotypically and functionally mature NK cells [23, 24] . In addition to these roles, IL-15 also can stimulate the migration of NK cells in vitro and enhances their adhesion to cultured endothelial cells [25] . We therefore hypothesized that virally induced IL-15 functionally assists in the migration of NK cells into the lung airways. We show here that an IL-15 deficiency results in a site-specific reduction in NK cells from the lung airway and an exacerbation of viral load at early time points post influenza infection. Additionally, exogenous IL-15 induces the specific migration of NK cells in vitro and in vivo. This IL-15dependent enhanced mobilization of NK cells to the lung airways correlates with decreased viral loads. Importantly, in the absence of NK cells, antigen-specific CD8 T cells fail to accumulate at the site of infection, providing a possible link between IL-15-mediated migratory effects of both the innate and adaptive immune responses to influenza infection and suggest therapeutic possibilities regarding the use of IL-15 to simultaneously regulate both arms of the immune system for improved responses to viral infection.