In MCMV-infected 129 or C57BL/6 immunocompetent animals, most of the systemic production of IFN-a/b and a significant proportion of that of IL-12p70 comes from pDCs [13, 14, 31] , which are not productively infected [13, 32] , and does not come from infected cells ( [13] and unpublished data). To our knowledge, the contribution of pDCs to IFN-a/b or other innate cytokine production has not been assessed in animals on a BALB/c genetic background, which are the most susceptible to MCMV infection. cDCs infected with MCMV in vitro have been reported to produce high levels of IFN-a/b [33, 34] , and more generally, any virus-infected cell could theoretically produce these cytokines. Therefore, the increase in the systemic levels of IFN-a/b observed in BALB/c animals could result either from a high activation of pDCs or from a more significant contribution to this function from other cell types or from the high numbers of infected cells in these animals [33, 34] . Therefore, we next compared the activation of pDCs for IFN-a/b or IL-12p70 production between BALB/c and Klra8 animals by intracellular staining for these cytokines on ex vivo isolated splenocytes ( Figure 1B ). Less than 1% of the pDCs were found to produce IFN-a/b or IL-12 in Klra8 as compared to 10%-12% in BALB/c mice. Consistent with previous reports on 129 or C57BL/6 animals [14, 35] , pDCs were the sole producers of IFN-a/b at all the time points examined in BALB/c and Klra8 mice (unpublished data). Both pDCs and cDCs contributed to the production of IL-12 in Klra8 mice. However, the high IL-12p70 serum levels observed in BALB/c mice could solely be attributed to pDCs ( Figure 1B and unpublished data). Therefore, a very high activation of pDCs for innate cytokine production was observed in BALB/c mice, which was drastically reduced in congenic animals endowed with efficient antiviral NK cell functions.