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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 5. DC-derived p38α signaling regulates reciprocal iTreg and Th1 differentiation in a TGF-β2-dependent manner.

Figure 5

(A) Expression of IFN-γ in OT-II T cells activated with CD103+ and CD103 MLN DCs and splenic DCs, in the presence of OVA (0.05 μg/ml), for 5 days, followed by intracellular cytokine staining. (B) T cells were transferred into Rag1–/– and p38αΔDC Rag1–/– mice, and expression of IFN-γ from donor cells in MLNs was analyzed at day 7. Right, the proportions of IFN-γ+ population among donor CD4+ T cells. (C) Expression of Foxp3 and IFN-γ in OT-II T cells stimulated with WT or p38α-deficient CD103+ DCs, in the presence of the indicated doses of OVA, for 5 days. (D) Gene expression in T cells from (C). (E) Expression of Foxp3 and IFN-γ in OT-II T cells stimulated with WT or p38α-deficient CD103+ DCs, in the presence of OVA (0.05 μg/ml), with or without TGF-β2 for 5 days. (F–G) Expression of Foxp3 (F) and IFN-γ (G) in OT-II T cells stimulated with WT or p38α-deficient CD103+CD11b+ or CD103+CD11b MLN DCs, in the presence of OVA (0.05 μg/ml), for 5 days. (H) RNA analysis of IFNγ and IL-17 expression from (FG). Data are representative of 2 (n=5 mice per group) independent experiments. Error bars indicate SEM.

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