Fig. 6: WDR77 dampens antiviral immune response in mouse primary cells.

a–f PEMs from WT, Wdr77^CKO and Mavs^-/- mice respectively were collected. PEMs were then stimulated for 6 h with or without VSV, SeV, poly(I:C), HSV or HT-DNA as indicated. Culture mediums were then collected and IFN-β was measured by ELISA (a). Ifnb1 (b), Ifna4 (c), Isg56 (d), Cxcl10 (e), Il-6 (f) induction were measured by qPCR (For a, IFN-β: **p = 0.0021 ****p < 0.0001, ****p < 0.0001, ^nsp = 0.0790, ^nsp = 0.9993 in sequence; for b, Ifnb1: all ****p < 0.0001, ^nsp = 0.1813, ^nsp = 0.8208 in sequence; for c, Ifna4: all ****p < 0.0001, ^nsp = 0.9997, ^nsp = 0.9998 in sequence; for d, Isg56: all ****p < 0.0001, ^nsp = 0.1378; For e, Cxcl10: all ****p < 0.0001, ^nsp = 0.5755, ^nsp = 0.7986 in sequence; for f, Il-6: ^nsp = 0.9872, ****p < 0.0001, ^nsp = 0.9932, ^nsp = 0.7531, nsp = 0.9849 in sequence). g BMDMs from WT, Wdr77^CKO and Mavs^-/- mice respectively were collected. BMDMs were then stimulated for 6 h with or without VSV, SeV, poly(I:C), HSV or HT-DNA as indicated. Ifnb1 induction was measured by qPCR. (All ****p < 0.0001, ^nsp = 0.1224, ^nsp = 0.9878 in sequence). h PEMs from WT, Wdr77^CKO and Mavs^-/- mice were collected respectively. PEMs were infected with or without SeV for 6 h. Cells were collected for subcellular fractionation, S5 fractions were subjected to native PAGE to examine IRF3 dimer. P5 fractions were subjected to SDD-AGE to examine MAVS aggregation and WCL were subjected to SDS-PAGE to examine IRF3 phosphorylation. Data are representative of two independent experiments with similar results (h), or three independent experiments (a–g) (mean ± SEM of three biological replicates). P-values were determined by two-way ANOVA (Tukey’s test) (a, b, g), two-way ANOVA (Šídák’s test) (c) or two-way ANOVA (Dunnett’s test) (d–f). n.s. indicates no statistical significance. Source data are provided as a Source Data file.