Fig. 6

The role of the JAK/STAT pathway in IFIT induction. A, B hBMECs were infected with JEV P3 for different time points, and the mRNA of STAT1 (A) and the protein of JAK1/p-JAK1, JAK2/p-JAK2, and STAT1/p-STAT1 (B) were measured. C The protein expression of JAK1/p-JAK1, JAK2/p-JAK2, and STAT1/p-STAT1 was measured in PRR-knockdown hBMECs under JEV infection. D, E IFN-β and IFN-λ1 mRNA levels were measured in PRR-knockdown hBMECs under JEV infection. F, G hBMECs were treated with rhIFN-β or rhIFN-λ1 protein for different time points, and JAK1/p-JAK1, JAK2/p-JAK2, and STAT1/p-STAT1 protein expression was measured. H hBMECs were treated with the carrier control DMSO or JAK inhibitor I at various concentrations for 72 h, and cell cytotoxicity was analyzed. I, J hBMECs were pretreated with carrier control DMSO or 5 μM JAK inhibitor I, followed by JEV P3 infection, and the mRNA of STAT1 (I) and the protein of JAK1/p-JAK1, JAK2/p-JAK2, and STAT1/p-STAT1 (J) were determined. K, L hBMECs were pretreated with the carrier control DMSO or 5 μM JAK inhibitor I, followed by JEV P3 infection, and IFIT mRNA (K) and protein (L) expression was measured. Data are represented as the mean values ± SEMs from three independent experiments. ***p < 0.001; ****p < 0.0001; ns: not significant