Fig. 4. Transgenic Bcl-x_L reduces γc abundance in RORγt^KO mice.

(A) Thymocytes of the indicated mice were incubated overnight at 37°C in cell culture medium. Cell viability was determined the next day by assessing propidium iodide (PI) exclusion by flow cytometry. Data are means ± SEM of five independent experiments with a total of five mice for each genotype. (B) TCRβ abundance on CD69⁻CCR7⁻ (population I) DP thymocytes of RORγt^KO and RORγt^KOBcl-x_L^Tg mice was assessed by flow cytometry. Histograms are representative of three independent experiments. (C) Surface γc abundance on TCRβ^low DP cells of WT, RORγt^KO, and RORγt^KOBcl-x_L^Tg mice was assessed by flow cytometry. Left: Histograms are representative of five independent experiments. Right: Data are means ± SEM of five independent experiments with a total of eight mice for each genotype. (D) Surface γc abundance on TCRβ^low DP thymocytes of the indicated mice was assessed by flow cytometry. Data are means ± SEM of three independent experiments with five WT, four RORγt^KO, three Mcl-1^Tg four Bim^KO, and three Noxa^KO mice. (E) Surface γc abundance on Mcl-1–deficient TCRβ^low DP thymocytes was assessed by gating on human CD4 reporter protein (hCD4)–positive cells in Mcl1^fl/flCD2-Cre mice. Data are means ± SEM of three independent experiments with five WT, four RORγt^KO, and three Mcl1^fl/flCD2-Cre mice. (F) Forward scatter (FSC) signals were determined in thymocytes of the indicated mice as a measure of cell size. Data are means ± SEM of four independent experiments with four mice for each genotype.