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. 2017 Dec 4;128(1):415–426. doi: 10.1172/JCI95837

Figure 4. The PI3K pathway controls γδT17 development.

Figure 4

(A and B) TCR-induced Akt phosphorylation in thymic γδT cells from Zap70–/– or Sykb–/– mice. Histograms show staining profiles of p-Akt in cells from WT (black lines) and mutant (red lines) mice, overlaid with nonstimulated profiles (shaded) after a 1-minute stimulation (A). MFI relative to nonstimulated controls (B). Thymocytes from adult Zap70–/– mice (n = 3) and neonatal Sykb–/– mice (n = 4) were used. (C–G) E15.5 fetal thymus from WT mice was cultured with vehicle alone (DMSO, 0.01%), IC87114 (1 μM), or SF1670 (2.5 μM) for 7 days (n = 5–11). (C) Flow cytometric profiles for CD3ε and TCRδ expression and absolute number of γδT cells. (D) Intracellular staining profiles for IL-17A production in γδT cells and absolute number of IL-17A–producing γδT cells (per lobe). (E) Intracellular staining profiles for RORγt expression in γδT cells and frequency of RORγt+ γδT cells. (F) Intracellular staining profiles for IFN-γ production in γδT cells and absolute number of IFN-γ–producing γδT cells (per lobe). (G) mRNA expression of Rorc, Sox13, and Sox4 in isolated γδT cells. Gene expression was normalized to β-actin (Actb) mRNA. (H) Number of Vγ4+ and Vγ6+ γδT cells. Data represent the mean ± SEM. *P < 0.05 and **P < 0.01, by unpaired t test (B and G) and 1-way ANOVA (C–F and H). Data represent 2 independent experiments (A and B) or a single experiment (G), or the combined results of 2 independent experiments (C–F and H).