Abstract
Accumulating data suggest that natural killer (NK) cells are involved not only in the innate antiviral response following infection, but also in shaping the quality of the adaptive immune response by modulating the functional properties of myeloid dendritic cells (DC) during the acute immune response to infection. In this role, NK cells ensure that only fully mature, immunogenic DCs gain access to inductive sites, where they might prime effective antiviral adaptive immune responses. However, increasing evidence now suggests that several aspects of this cross-talk between NK cells and DCs are compromised during HIV infection, potentially contributing to immune dysfunction.