Fig. 2
Propranolol dose-response effects on NK cells phenotype, activation, and regulatory receptor expression. Expanded NK cells were treated with increasing concentrations of propranolol (0, 10, 20, 50, 100, or 200 ng/mL) in the absence or presence of an inflammatory stimulus (PMA plus ionomycin, brefeldin A, and monensin). (A) Total NK cells (CD3⁻CD56+). (B,C) Cytotoxic (CD56dimCD16bright) and effector (CD56brightCD16dim) subset. (D–F) Activation (CD38), differentiation (CD57), and degranulation (CD107a) markers. (G) Senescence marker KLRG1. (H–J) Regulatory receptors LAG-3, NKG2A, and NKG2D. (K–L) Immune-exhaustion markers PD-1 and TIM-3. Data are presented as mean ± SEM from n = 4 untrained and n = 5 endurance-trained donors. * P < 0.05 versus untreated control; & P < 0.05 versus PMA; # P < 0.05 between PMA-stimulated and unstimulated at the same dose. All comparisons were determined using Bonferroni post hoc tests following a significant interaction effect detected by two-way ANOVA. CD, cluster of differentiation; KLRG1, killer cell lectin-like receptor subfamily G member 1; LAG-3, lymphocyte-activation gene 3; NK, natural killer; NKG2A, natural killer group 2, member A; NKG2D, natural killer group 2, member D; PD-1, programmed death-1; PMA, phorbol 12-myristate 13-acetate; TIM-3, T-cell immunoglobulin and mucin-domain containing-3.
