A significant finding of our work is that NK cells immigrating into the lung airways are partially required for substantial trafficking of influenza-specific effector CD8 T cells to this location. We found that NK cells are necessary for the optimal accumulation of antigen-specific CD8 T cells, important effectors of eventual viral clearance [4, 5] , at the site of infection, since depletion of NK1.1-expressing cells resulted in a significant decrease in the number of influenza-specific CD8 T cells in the BAL. A subpopulation of CD8 T cells has been shown to express NK1.1 upon activation [50] , and while these cells were detected in the lung parenchyma of influenza-infected C57Bl/6 mice, they comprised less than 1% of the NP-tetramer+ CD8 T cells at this site alone and were never detected in the lung airways. This and the fact that the reduction of activated, influenza-specific CD8 T cells was observed only in the lung airways, and only at later time points post infection lead us to believe that direct depletion of NK1.1-expressing CD8 T cells cannot account for this reduction in treated mice. These data strongly suggest that NK1.1 + cells in the lung airways are requisite for the subsequent accumulation of influenza-specific CD8 T cells in the BAL and implicate IL-15mediated NK cell migration into the lung airways as a link between the innate and adaptive responses to influenza infection. We currently favor a model in which NK cells migrate directly to influenza-induced IL-15 in the lung airways, and, CD8 T cell trafficking, in turn, occurs to both IL-15 directly and to chemotactic factors produced by NK cells already present at the site. A positive feedback loop in which NK cells responding to IL-15 induce further expression of IL-15 by dendritic cells for the stimulation of CD8 T cells is an additional possibility [51] . Moreover, IL-15 has also been shown to modulate chemokine and chemokine receptor expression by NK cells and T cells [52, 53, 54] . As IL-15 deficiencies also cause reductions in CD8 T cell accumulation in the BAL [19] , chemotactic potential of IL-15 for NK cells presented here provides a possible link between IL-15-mediated effects of both the innate and adaptive immune responses to influenza infection. Future work will attempt to tease out the roles of direct and indirect migration of both NK cells and CD8 T cells to IL-15 following influenza infection.