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. 2018 Dec 28;116(3):982–987. doi: 10.1073/pnas.1807484116

Fig. 3.

Fig. 3.

Insufficient SMAD2 activation and overactivated SMAD3 under TGFβ pathway restrains TH17 differentiation. (A and B) Histograms (A) and mean fluorescence intensity (MFI) quantification (B) of TGFβ receptor I and II staining on CD4-gated cells from splenocytes of PP2A WT and cKO mice. (C) Enriched CD4+ T cells from PP2A WT and cKO were stimulated with 10 ng/mL TGFβ as indicated, whole-cell lysates were probed with the indicated antibodies in the immunoblots. (D and E) Flow cytometry (D) and quantification (E) of TH17 polarization with ectopic expression of Vector, WT, 2SA, and 2SD of SMAD2 in WT naïve CD4+ T cells. GFP-expressing cells were gated for analysis on day 3. (F and G) Flow cytometry (F) and quantification (G) of TH17 polarization with ectopic expression of Vector, WT, 2SA, and 2SD of SMAD3 in WT naïve CD4+ T cells. GFP expressing cells were gated for analysis on day 3. Each symbol represents an individual mouse (n = 4). Error bars show mean ± SEM. Data are representative of three independent experiments (C) or two independent experiments with two replicates (D and F). *P < 0.05; **P < 0.01; NS, not significant.