Fig. 3
From: Pharmacologic inhibition of IL11/STAT3 signaling increases MHC-I expression and T cell infiltration
IL11 activates STAT3 to inhibit IFNγ-induced STAT1 signaling and MHC-I expression. A, B Immunoblot of STAT1/3 (total and phosphorylated) in IL11-treated (100/200 ng/ml) MC38 with/without IFNγ induction (10 ng/ml). GAPDH as internal reference. STAT1 phosphorylation ratio was calculated. Data presented as means ± SD from three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, t test. C mRNA expression of CXCL9, H2-D1, H2-K1 in IL11-treated (100/200 ng/ml) MC38 with/without IFNγ induction (10 ng/ml). Data presented as fold change to control group and means ± SEM from three independent experiments. *P < 0.05, **P < 0.01, t test. D, E Integrated graph and MFI (mean fluorescence intensity) of flow cytometry analysis on cell surface H2-Kb/Db of IL11-treated (100/200 ng/ml) MC38 with/without IFNγ induction (10 ng/ml). Data presented as fold change to control group and means ± SEM from three independent experiments. *P < 0.05, t test. F Representative images of murine intestinal organoids under IL11 stimulation. Scale bar, 400 μm. (G)-(H) Immunoblot of STAT1/3 (total and phosphorylated) in IL11-treated (100 ng/ml) murine intestinal organoids with/without IFNγ induction (10 ng/ml). STAT1 phosphorylation ratio was calculated. Data presented as means ± SD from three independent experiments. **P < 0.01, ***P < 0.001, t test. I–K mRNA expression of CXCL9, H2-D1, H2-K1 in IL11-treated (100/200 ng/ml) Stat3fl/fl organoids (I), HT-29 cells (J) and RKO cells (K) with/without IFNγ induction (10 ng/ml). Data presented as fold change to control group and means ± SEM from three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, t test