In the early phase of MCMV infection there is a tight temporal relationship between the activation and exertion of effector functions between NK cells and pDCs because the production of IFN-a/b by pDCs promotes NK cell proliferation and cytotoxicity [13, 24] . However, the impact of NK cell functions on the pDC response to MCMV remains unexplored. The goal of this study was therefore to evaluate the effect of efficient NK cell responses on pDC IFN-a/b production and on the development of the adaptive immune responses of the host. C57BL/6 mice are able to mount NK cell responses that can control MCMV replication very efficiently, due to their expression of the Ly49H activating receptor, which endows NK cells with the ability to recognize and kill viral-infected cells expressing the viral ligand m157 (reviewed in [1] ). Although the NK cells from BALB/c and other strains of mice lacking the Ly49H gene are strongly activated for the acquisition of the cytotoxic machinery and for the production of IFN-c early after MCMV infection, they fail to recognize and kill infected cells and can therefore be considered inefficient. Inbred mouse strains that are resistant or sensitive to MCMV infection in an NK cell-dependent manner differ in many other immune parameters, including major histocompatibility (MHC) haplotype as well as DC subset frequency and function [25] . Therefore, rigorous evaluation of the impact of NK cell responses on pDC and adaptive responses requires comparison between mice of the same genetic background differing only in the ability of their NK cells to control the infection. For this, we took advantage of the fact that the Ly49H/m157 activation axis is sufficient for NK cell control of MCMV when introduced into the BALB/c genome [26] . The response of pDCs and CD8 T cells to MCMV were therefore compared between BALB/c mice (Ly49H À ) and animals on the BALB/c background that are congenic for the C57BL/6 natural killer complex and in particular for Ly49H (C.B6-Klra8 Cmv1-r /UwaJ mice, hereafter named Klra8 [27] ). This system thus provides a unique model to study antiviral immune responses in vivo in the context of both efficient (Ly49H þ ) and inefficient (Ly49H À ) NK cell activation, in the absence of any broad defect in NK cell development or activity that may affect the homeostasis or functions of other immune cells. This system allowed us to demonstrate, to our knowledge for the first time, that NK cells accelerate CD8 T cell responses against a viral infection in vivo. Moreover, we identified the underlying mechanismthe ability of NK cells to limit pDC IFN-a/b production to levels not immunosuppressive to the host-which itself results from the early control of viral replication.