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. 2022 Aug 16;13:4822. doi: 10.1038/s41467-022-32401-1

Fig. 2. Irf8 mediates activation of Sting-Irf3 axis independent of its transcriptional activity.

Fig. 2

a Immunoblot analysis of the indicated proteins in WT, Irf8−/− or Irf3−/− BMDMs un-infected or infected with HSV-1 (left) or VACV (right) for the indicated times. b Immunostaining showing Irf3 (green) in wild-type or Irf8−/− BMDMs infected with HSV-1 for 6 h. Scale bars, 100 μm. The number of cells with Irf3 translocation was counted from three random fields (lower histogram). Graph shows mean ± SEM, n = 3 independent samples. Data were analyzed by unpaired two-tailed Student’s t-test. c Irf8−/− BMDMs were reconstituted with wild-type Irf8 or the indicated mutants. The cells were infected with HSV-1, or treated with LPS (10 ng/mL) plus IFN-γ (50 ng/mL) for 6 h before qPCR analysis of the mRNA levels of the indicated genes. d Irf8−/− BMDMs were reconstituted with wild-type Irf8 or the indicated mutants. The cells were infected with HSV-1 for the indicated times, and then ELISA analysis of Ifn-β and IP-10 secretion was performed. Data in c, d are presented as mean, n = 2 biological replicates. Data were analyzed by unpaired two-tailed Student’s t-test. Source data are provided as a Source data file.