Figure 7
Figure 7. Activation of the PI3K pathway is required for IL-7–induced cell-cycle progression and surface Glut-1 expression. (A) rIL-7–stimulated CD4+ RTEs (10 ng/mL) were cultured in the continuous presence of varying concentrations of the PI3K activity inhibitor LY294002 (0-15 μM). Cell-cycle progression, assessed by Ki67 expression and DNA content, was monitored at 96 hours after gating on viable cells. Viability, monitored by FSC/SSC profiles, was assessed on the total ungated population of lymphocytes. Data are representative of results obtained in 2 independent experiments. (B) rIL-7–stimulated CD4+ RTEs (10 ng/mL) were cultured in the absence or presence of LY294002 (15 μM) for 5 days. Tyr694 phosphorylation of STAT5 and surface Glut-1 expression were assessed and representative histogram plots, relative to control fluorescence (shaded histograms), are shown.

Activation of the PI3K pathway is required for IL-7–induced cell-cycle progression and surface Glut-1 expression. (A) rIL-7–stimulated CD4+ RTEs (10 ng/mL) were cultured in the continuous presence of varying concentrations of the PI3K activity inhibitor LY294002 (0-15 μM). Cell-cycle progression, assessed by Ki67 expression and DNA content, was monitored at 96 hours after gating on viable cells. Viability, monitored by FSC/SSC profiles, was assessed on the total ungated population of lymphocytes. Data are representative of results obtained in 2 independent experiments. (B) rIL-7–stimulated CD4+ RTEs (10 ng/mL) were cultured in the absence or presence of LY294002 (15 μM) for 5 days. Tyr694 phosphorylation of STAT5 and surface Glut-1 expression were assessed and representative histogram plots, relative to control fluorescence (shaded histograms), are shown.

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