In vivo NK-cell function. (A) In vivo killing of MHC class I–deficient splenocytes. Splenocytes from WT or Tap1-deficient mice (Tap1^−/−) were isolated, stained with 2 different concentrations of the fluorescent dye CFSE, and transferred intravenously into the recipient mice indicated (Tap1^−/−, WT, or Itgb2^Jkr/Jkr). Two days after transfer, the frequency on each CFSE⁺ population was assessed by flow cytometry. Data are represented as the percentage of killing of TAP-1^−/− cells. (B-C) Itgb2^Jkr/Jkr mice are not susceptible to MCMV infection. (B) Viral loads in spleens of C57BL/6J resistant mice, BALB/cByJ susceptible mice, and Itgb2^Jkr/Jkr mutant mice were tested 5 days after infection with 10⁵ PFU of MCMV inoculated intraperitoneally; nd, not detectable; n = 6 for each genotype. (C) Sera of C57BL/6J and Itgb2^Jkr/Jkr mice infected with 10⁵ PFU of MCMV were collected at 36 hours after infection, when systemic cytokines peak. IFN-γ, IL-12p70, and IL-12p40 were titrated by enzyme-linked immunosorbent assay performed on the serum; n = 6 for each genotype. These graphs are representative of 1 experiment of 2.