Type I IFN influences Ccl3 production during mCMV. (A) Scheme of the experiment. Heterozygous CCL3-EASER mice were i.v. infected with WT Smith- or ∆m157-mCMV and analyzed 16 h after infection. Ccl3 promotor and transcriptional activities of NK cell were analyzed by flow cytometry according to tdTomato and Venus signals, respectively, after 4 h of in vitro stimulation in the presence of monensin and brefeldin A. (B) Frequency of tdTomato⁺ NK cells from WT Smith- or ∆m157-infected CCL3-EASER mice and tdTomato MFI. (C) Frequency of Venus⁺ NK cells from WT Smith- or ∆m157-infected CCL3-EASER mice and Venus MFI. (D) Scheme of the experiment. Homozygous CCL3-EASER mice were i.p. treated with 200 µg of anti-IFNAR-1 antibody (clone MAR1-5A3) or irrelevant isotype control. 1 h later, mice were infected i.v. with mCMV and analyzed as previously described in A. (E) Frequency of tdTomato⁺ NK cells from isotype- or IFNAR-1–treated CCL3-EASER mice and tdTomato MFI. (F) Frequency of Venus⁺ NK cells from isotype- or IFNAR-1–treated CCL3-EASER mice and Venus MFI. (G) Representative XY plots of Venus and tdTomato channel intensity of liver NK cells gated on tdTomato-positive cells. Dotted lines represent the simple linear regression of the correlation between Venus and tdTomato channel intensity (gray: isotype; orange: IFNAR-1). (H) Comparison of linear regression from isotype- or IFNAR-1–treated CCL3-EASER mice. Color code as described in G. Black dotted line indicates tdT₅₀: point of half of tdTomato channel intensity from the isotype control group. In B, C, E, and F, data is presented as mean ± SD and representative of at least three mice per group of two independent experiments. Each experiment is indicated with different symbols within the column plots: (1) circles, (2) triangles. Unpaired nonparametric Mann–Whitney U-test was used: ns, not significant; *P < 0.05; **P < 0.01; ***P < 0.001. In G correlation test was used, two-tailed P value, Pearson r with 95% confidence interval.