Not only might there be different cellular sources of IL-15 at different times after infection, but IL-15 signaling in NK cells could also be regulated by the context in which IL-15 is presented. At least one isoform of IL-15 is known to enter the cell secretory pathway and could therefore be released as a soluble molecule [47, 48] . These data lend the idea that soluble IL-15 could bind heterotrimeric receptors on NK cells. However, IL-15 is also known to be transpresented to NK cells, and indeed, this mode of signaling appears to be most important for IL-15-mediated NK cell survival [49] . While IL-15Ra is dispensable for NK cell survival, IL-15Ra is thought to be an important component in signaling the migration of CD16 2 human NK cells into the endometrium, since this particular NK cell population expresses higher levels of this receptor component than CD16 + NK cells that do not migrate to IL-15 [36] . In our studies, IL-15Ra was only expressed on a relatively low proportion of NK cells in the lung airways of influenza-infected animals ( Figure 1 ). In contrast, CD122 signaling appears to be important for NK cell migration to IL-15 as this receptor chain is down regulated on NK cells exposed to IL-15c in vivo ( Figure 3 ). Thus, we consider it likely that signaling through IL-15Ra is not essential to IL-15-mediated of migration of NK cells to the lung airways. Therefore, future work is needed to identify the IL-15-producing cell population(s) and the mechanism of migration to this cytokine in order to target this response for eventual applications in influenza vaccines and treatments.