Enhanced IFN-I production and viral clearance upon LCMV infection in NFAT5-deficient mouse models. (A and B) Analysis of IFNα concentration in serum (A) and viral load in the spleens (B) of Nfat5^+/+ Vav-Cre (n = 24) and Nfat5^fl/fl Vav-Cre (n = 21) mice 2 d after acute infection with LCMV strain Docile (2 × 10² PFU per mouse). (C and D) mRNA levels of Ifnb1 and the viral gene LCMV NP in splenic pDCs (C) and peritoneal macrophages (D) of Nfat5^+/+ Vav-Cre (n = 19) and Nfat5^fl/fl Vav-Cre (n = 16) mice 2 d after infection. pDCs were isolated by flow cytometry cell sorting using the gating strategy shown in Fig. S2 A. (E–G) Analysis of IFNα concentration in serum (day 2; E), viral load in spleen (day 7; F), and mRNA levels of the viral gene LCMV NP in peritoneal macrophages (day 7; G) in Nfat5^+/+ LysM-Cre (n = 19 in E and G; n = 10 in F) and Nfat5^fl/fl LysM-Cre (n = 17 in E and G; n = 10 in F) mice after acute infection with LCMV. Error bars in A–G show the mean ± SEM. Data in A–D comprise three independent in vivo infection experiments. Data in E–G comprise two independent in vivo infection experiments. Statistical significance was determined with an unpaired t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.