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. 2019 Feb 19;10:251. doi: 10.3389/fimmu.2019.00251

Figure 2.

Figure 2

Loss of JAK1 attenuates JAK–STAT signaling in tumor cells. (A,B) B16/OVA, B16/OVA-JAK1−/−, and B16/OVA-JAK1−/−-mutJAK1 were stimulated with mouse (m)IFN-γ (100 ng/mL) (A) or mIFN-α4 (500 ng/mL) (B), and pSTAT1 level was analyzed by flow cytometery 0.5 h later. MHC-I and PD-L1 expression was analyzed by flow cytometry 24 h after stimulation. MHC-I and PD-L1 expression in B16F10 and MC38 cells with JAK1 deficiency were observed after stimulation with mIFN-α4 (500 ng/mL) (C,D). Data are presented as mean ± SEM. **P < 0.01 vs. B16- OVA/B16F10/MC38 control group; ##P < 0.01 vs. B16/OVA/B16F10/MC38 + IFN-α group.