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. Author manuscript; available in PMC: 2014 Jul 15.
Published in final edited form as: J Immunol. 2013 Jun 10;191(2):650–659. doi: 10.4049/jimmunol.1300398

Figure 3. DC-derived p38α signaling promotes iTreg generation by regulating TGF-β2 expression in CD103+ DCs.

Figure 3

(A) RNA analysis of CD103+ and CD103– MLN DCs and splenic DCs. (B) RNA analysis of WT or p38α-deficient CD103+ DCs. (C) Phosphorylation of Smad3 in OT-II T cells stimulated with WT or p38α-deficient CD103+ DCs, in the presence of OVA (0.05 μg/ml), for 2 days. (D) RNA analysis of OT-II T cells activated with WT or p38αΔDC DCs, in the presence of OVA (0.05 μg/ml), for 5 days. (E) Expression of Foxp3 in OT-II T cells activated with WT or p38αΔDC DCs, in the presence of OVA (0.05 μg/ml), with or without TGF-β2 for 5 days. (F) Phosphorylation of Smad3 in OT-II T cells stimulated with WT or p38αΔDC DCs, in the presence of OVA (0.05 μg/ml), with or without TGF-β2 for 2 days. (G) Expression of Foxp3 in OT-II T cells activated with WT or p38αΔDC DCs, in the presence of OVA (0.05 μg/ml), with or without αTGF-β for 5 days. (H) Expression of Foxp3 in WT and CD4-dnTGFβRII (DNR) polyclonal T cells activated with WT or p38αΔDC DCs, in the presence of αCD3 (0.1 μg/ml), for 5 days. Data are representative of 2 (n=4 mice per group) independent experiments. Error bars indicate SEM.

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