DC-to-MC communication critically contributes to hapten-specific T cell–induced skin inflammation. (A) Skin inflammation was induced by i.d. injection of T cells from DNFB-sensitized WT donor mice into DNFB-treated ear skin of recipient mice as follows: group G1: CD11c-Cre⁻ iDTR control mice treated with DT 48 h after DNFB; group G2: CD11c-Cre⁺ iDTR mice treated with DT 48 h after DNFB; and group G3: CD11c-Cre⁺ iDTR mice treated with DT at 4 h and 48 h after DNFB. (B) T cell–induced ear swelling was measured at the indicated time points. Data are represented as mean ± SD. *, P < 0.005 related to group 1; ‡, P < 0.05 related to group 2; #, P < 0.005 related to group 2; n = 8/group. (C and D) CD11c⁺MHCII^hi DC numbers (C) and CD117⁺FcεRI⁺ MC numbers (D) were quantified 24 h after last DT injection by flow cytometry in comparison to not DT-treated Cre⁻ controls. ***, P < 0.001; n = 5/group. (E) MC-deficient Mcpt5-Cre⁺ R-DTA⁺ mice and Mcpt5-Cre⁺ R-DTA⁺ × CD11c-eGFP/DTR mice were reconstituted with WT CTMCs in one ear and MHCII^−/− CTMCs in the contralateral ear (n = 7/group). 4 wk after reconstitution, recipient mice were sensitized and challenged with DNFB. In Mcpt5-Cre⁺ R-DTA⁺ × CD11c-eGFP/DTR mice, DCs were locally depleted by i.d. injection of DT into the ear pinnae 4 h after DNFB. (F and G) Ear swelling was measured 24 h and 48 h after DNFB (F), and cytokines were quantified in protein extracts of challenged ear skin 48 h after DNFB (G) using a bead-based multiplex assay. *, P < 0.05; **, P < 0.01; ***, P < 0.001.