αβ T cells and ILCs can compensate absent Tγδ17 cells. (A) Frequencies of indicated cell populations among IL-17A⁺ cells. Tcrd-GDL ctrl.: nondepleted; Tcrd-GDL 8w: 8 wk after γδ T cell depletion. Shown are pooled data from two experiments with each n = 2–4 mice per group, mean ± SD. (B) Frequencies of indicated cell populations among IL23R-GFP⁺ ear skin lymphocytes from heterozygous IL23R-GFP reporter mice. Pooled data from two experiments with each n = 2–3 mice per group, mean. (C) Ear thickness and disease score over time in control and IMQ-treated groups. IMQ treatment started 9 wk after γδ T cell depletion. Graphs show pooled data from two experiments, each n = 1–3 mice per group (total numbers of mice: five Tcrd-GDL DTx IMQ; six Tcrd-GDL ctrl. IMQ; six Tcrd^−/− IMQ; two Tcrd-GDL DTx Vas; three Tcrd-GDL ctrl. Vas; three Tcrd^−/− Vas); two-way ANOVA with Bonferroni posttests, mean ± SD. (D) Composition of IL-17A–producing lymphocytes from psoriatic ear skin draining lymph nodes day 8 of IMQ-psoriasis, 9 wk after γδ T cell depletion. Frequencies of indicated cell populations in nondepleted Tcrd-GDL control (ctrl.) compared with Tcrd-GDL mice that were treated with DTx 9 wk before psoriasis induction (DTx 9 w). Data shown are from one representative experiment out of two independent experiments with each n = 2–3 mice per group. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.