Figure 3. DETC produce IL-17A upon skin injury in vivo.

(A) Increased frequency of IL-17A–producing Vγ3⁺ DETC in wounded skin. Epidermal cells were isolated from skin areas directly surrounding wounds or from nonwounded skin, 18 hours after wounding. Intracellular IL-17A production was analyzed by flow cytometry. Data are pooled and shown as the mean ± SEM of Vγ3 cells producing IL-17A from independent analyses of 4 mice and are expressed as percentage of Vγ3⁺ cells producing IL-17A. **P < 0.01. (B) Signaling through the Vγ3Vδ1 TCR is required for DETC-mediated IL-17A expression in vivo. Vγ3⁺ DETC from WT and epidermal TCRβ⁺ cells from Tcrd^–/– mice were isolated and sorted from the epidermis of wounded and nonwounded skin areas 18 hours following skin injury. IL-17A was measured by qPCR. Data are pooled and shown as mean ± SEM from 3 independent experiments with at least 4 mice per genotype per experiment. (C) RORγt increases in DETC upon skin injury. DETC were isolated 12 hours following skin injury from nonwounded and wounded skin areas and were stained for RORγt. Cells are gated on Vγ3⁺Thy1.2⁺. (D) Ifng is upregulated upon skin injury. Vγ3⁺ DETC were isolated and sorted from the epidermis of wounded and nonwounded skin areas 18 hours following skin injury. Ifng was measured by qPCR. Data are pooled and shown as mean ± SEM from 3 independent experiments with at least 4 mice per genotype per experiment.