Fig. 2

TNF-α inhibits EBV reactivation by acting on TNFR1 receptors. (A) Raji cells were transfected with control (NC) siRNA or TNFR1 siRNA. The cell lysates were harvested, and western blotting was performed with TNFR1 antibodies. (B) Raji cells were directly treated with different concentrations of the TNFR1 inhibitor R-7050. The cell lysates were harvested, and western blotting was performed with the indicated antibodies. (C) After TNFR1 was knocked down with siRNA, the cells were treated with TPA (20 ng/ml) or TNF-α (200 ng/ml) for 24 h. The cell lysates were harvested, and western blotting was performed with the indicated antibodies. (D) After treatment with the TNFR1 inhibitor R-7050 (10 mM), Raji cells were induced with TPA (20 ng/ml) and TNF-α (200 ng/ml) for 24 h. The cell lysates were harvested, and western blotting was performed with the indicated antibodies. (E) For FC analysis of apoptosis, Raji cells were treated with TPA (20 ng/ml) or TNF-α (200 ng/ml) for 24 h. (F) For FC analysis of apoptosis, LCL cells were treated with TPA (20 ng/ml) or TNF-α (200 ng/ml) for 24 h. (G) The fluorescent ROS probe DCFH-DA was added to Raji cells treated with TPA (20 ng/ml) or TNF-α (200 ng/ml) for 24 h. (H) Raji cells were transfected with control (NC) siRNA or TNFR1 siRNA. After that, Raji cells were induced with TPA (20 ng/ml) and TNF-α (200 ng/ml) for 24 h and harvested for immunofluorescence assays using Rta (red) and Zta (green) antibodies. The data shown are representative of three independent experiments. The data are presented as the means ± SDs. *P < 0.05; **p < 0.01 by one-way ANOVA.