Figure 7. p38α is required for Aldh1a2 expression in CD103⁺ DCs and DC-mediated imprinting of gut homing receptors on responding T cells.

(A) RNA analysis of Aldh1a2 from CD103⁺ and CD103^– MLN DCs and splenic DCs. (B) Expression of Aldh1a2 in CD103⁺ DCs from WT or p38α^ΔDC mice. (C) Naïve OT-II T cells (Thy1.1⁺) were transferred into WT or p38α^ΔDC mice that were subsequently fed with OVA in the drinking water for 5 days, followed by analysis of α4β7 and CCR9 expression on the donor population in MLNs. Right, the proportions of α4β7⁺ and CCR9⁺ populations among donor CD4⁺ T cells. (D) Expression of α4β7 and CCR9 on OT-II T cells stimulated with WT or p38α-deficient CD103⁺ DCs, in the presence of OVA (0.05 μg/ml), for 5 days. (E, F) Expression of α4β7 (E) and CCR9 (F) on OT-II T cells stimulated with WT or p38α-deficient CD103⁺ DCs, in the presence of OVA (0.05 μg/ml), with or without RA for 5 days. (G) Expression of Foxp3 in OT-II T cells activated with WT or p38α-deficient CD103⁺ DCs, in the presence of OVA (0.05 μg/ml), with or without RA for 5 days. (H) Proposed model of p38α-dependent programming of CD103⁺ mucosal DCs to mediate reciprocal differentiation of Th1 and iTreg cells, and the induction of gut-homing receptors on T cells. Data are representative of 2 (A, C, E, F, n≥5 mice per group; G, n=3 mice per group) and 3 (B, D n=4 mice per group) independent experiments. Error bars indicate SEM.