Resolution of virus infections relies on the orchestrated activation of dendritic cells (DC), CD4 T cells and killer T cells. We have known for some time that CD4 T cells contribute to killer T cell immunity, but how CD4 T cells, DC and killers interact in vivo is still unclear. Using a model of peripheral virus infection, Sammy’s group found that CD4 T cells contributed to CTL immunity by amplifying the IFN-α/β-induced provision of IL-15 by DC to CTL. Building upon these novel findings, they are currently dissecting the molecular mechanisms.