Figure 7
Figure 7. IL-15–induced proliferation of SD-1 cells is mediated via the MEK/ERK signaling pathway. SD-1 cells were treated with (A) 10 μM ERK1/2 inhibitor (dashed lines), (B) 100 μM STAT5 inhibitor (dashed lines), (C) 10 μM MEK inhibitor (dashed lines), (D) 5 µM NF-κB inhibitor (IKK-2 inhibitor IV), or 20 µM PI3K inhibitor (LY 294002) or matched vehicle controls (0.1% DMSO) (solid lines) with (solid symbols) or without (open symbols) additional IL-15 (25 ng/mL). Viable cell numbers were determined using trypan blue. Data are mean ± standard error of the mean. Unpaired Student t tests were used to compare cell counts at 72 and 96 hours in drug-treated IL-15 vs no IL-15 groups. *P < .05, **P < .01, n.s = no significant difference. Vehicle-treated IL-15 vs no IL-15 groups showed a significant (P < .05) increase in cell numbers with IL-15 treatment at 72 and 96 hours as previously shown (Figure 2C). Representative graphs of 3 independent experiments are shown.

IL-15–induced proliferation of SD-1 cells is mediated via the MEK/ERK signaling pathway. SD-1 cells were treated with (A) 10 μM ERK1/2 inhibitor (dashed lines), (B) 100 μM STAT5 inhibitor (dashed lines), (C) 10 μM MEK inhibitor (dashed lines), (D) 5 µM NF-κB inhibitor (IKK-2 inhibitor IV), or 20 µM PI3K inhibitor (LY 294002) or matched vehicle controls (0.1% DMSO) (solid lines) with (solid symbols) or without (open symbols) additional IL-15 (25 ng/mL). Viable cell numbers were determined using trypan blue. Data are mean ± standard error of the mean. Unpaired Student t tests were used to compare cell counts at 72 and 96 hours in drug-treated IL-15 vs no IL-15 groups. *P < .05, **P < .01, n.s = no significant difference. Vehicle-treated IL-15 vs no IL-15 groups showed a significant (P < .05) increase in cell numbers with IL-15 treatment at 72 and 96 hours as previously shown (Figure 2C). Representative graphs of 3 independent experiments are shown.

Close Modal

or Create an Account

Close Modal
Close Modal