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. 2019 Feb 15;38(6):e99595. doi: 10.15252/embj.201899595

Figure 3. LIF activates STAT4 to block Th17‐cell differentiation in the mouse colitis model and in vitro .

Figure 3

  1. Colons obtained from WT or Stat4‐KO mice on day 10 of the colitis model induced as in Fig 2A were immunostained with an antibody against phosphorylated STAT4. Scale bar, 50 μm.
  2. Immunoblot analysis of STAT4 phosphorylation in spleen tissue from colitis mice.
  3. FACS staining of LPLs isolated on day 10 from the colon of WT or Stat4‐KO colitis mice receiving PBS or LIF (n = 4 per group). The percentage of IL‐17A+ and/or IFNγ+ CD4+ T cells in vivo was analyzed.
  4. Quantitative expression of Il17a mRNA in MLNs and LNs from colitis mice treated as described in Fig 2A (n = 3 per group).
  5. FACS staining of WT and Stat4‐KO naïve CD4+ T cells treated with LIF (50 ng/ml) on day 4 of induction into Th17‐cell subsets.
  6. qPCR analysis of Th17‐related genes in WT or Stat4‐KO naïve CD4+ T cells on day 4 of induction into Th17‐cell subsets in the absence or presence of LIF (n = 3 per group).
  7. FACS staining of WT or Stat4‐KO naïve CD4+ T cells treated with LIF (50 ng/ml) on day 4 of induction into nonpathogenic or pathogenic Th17 cells. The data are representative of three independent experiments.
Data information: *P < 0.05, **P < 0.01, and ***P < 0.001 (Student's t‐test). Error bars represent the SEM.Source data are available online for this figure.