We and others have shown that following influenza infection, IL-15 message and protein is increased in the lung airways [19, 27] . Because this IL-15 expression was rapidly induced by influenza infection and reached significant levels as early as day 3 post infection (p.i.) [19] , we hypothesized that influenza-induced IL-15 expression may be an important mediator of NK cell responses to influenza infection. We therefore first sought to determine whether NK cells responding to influenza infection were capable of receiving signals from this locally produced IL-15. To this end, lymphocytes were isolated from the lung airways of influenzainfected animals via BAL, and CD3 2 , NK1.1 + NK cells were analyzed for the expression of IL-15 receptor components by flow cytometry. The IL-15 receptor is a heterotrimer, consisting of the common gamma chain (CD132), the shared IL-2/IL-15Rb chain (CD122), and the specific IL-15Ra chain [28] . To date the majority of biological effects of IL-15 on NK cells, however, are mediated through the paired co-expression of CD122 and CD132 [29, 30, 31] , while IL-15Ra is only required by accessory cells which present IL-15 to respondent cells, a mechanism referred to as trans-presentation [32] . However, some groups have suggested that IL-15Ra expression alone contains some signaling moieties which may participate in distinct biological functions [27] . Therefore it is important to establish the kinetics of IL-15 receptor component expression and IL-15 signaling potential on NK cells in our model. NK cells are known to respond rapidly to influenza infection and continue accumulating in the lung airways through day 5 p.i. ( [13] and data not shown). Since we wished to specifically evaluate recent NK cell immigrants responding to the airway inflammation resulting from influenza infection, we restricted our analyses of NK cell kinetics to before and up to day 4 p.i.. NK cells were first detected in the BAL at day 2 post influenza infection (albeit at a low frequency, ,0.1-0.6% of lymphocytes, Figure 1A and Figure 2A ) but were completely absent in control mock-infected animals (data not shown). Despite the low frequency of NK cells in the lung airway at this early time point, one fifth consistently expressed IL-15Ra. Additionally, 30-40% of them expressed CD122 and CD132 ( Figure 1B ). By day 3 p.i., when NK cells represented a much more discernible population (,2-3% of lymphocytes, Figure 1A & 2A), greater than 90% of these gated cells expressed CD122 and CD132, and expression levels of these receptors on a per-cell basis increased over time as indicated by a higher median fluorescence intensity by day 4 p.i. ( Figure 1B ) and consistent with evidence that expression of IL-15R components is induced by activating stimuli [33] . Expression of IL-15Ra however, was variable but consistently much lower that the expression levels of CD122 and CD132. This biased expression of CD122/132 receptor chains over IL-15Ra and enhanced IL-15 levels [19] following influenza infection, indicate that NK cells accumulating at the site of influenza infection are capable of responding to locally produced IL-15 via the trans-presentation pathway.