Modeling and Simulation Based Analysis of Multi-Class Traffic with Look-Ahead Controlled Vehicles

Additional file 7: Fig. S7. TLR and PTEF-b inhibition impairs TLR-mediated HIV reactivation. a TLR ligands reactivate HIV in an NF-κB-dependent manner. Treatment of THP-1/HIV (HA3) cells with TNF-α (10 ng/mL) or TLR ligands (Pam3CSK4 at 0.1 µg/mL, HKLM at 108 cells/mL, poly (I:C) at 10 µg/mL, LPS at 1 µ/mL, flagellin at 1 µ/mL, FSL-1 at 1 µg/mL, imiquimod at 10 µg/mL, ssRNA40 at 5 µg/mL, and ODN2006 at 5 µM) for 16 h after a 2-h pre-incubation with either 100 µM of IKKγ NEMO binding domain inhibitory peptide (red bars; Inh Pep) or equivalent amount of the control peptide (blue bars; Imgenex) (X-axis). Y-axis represents % of GFP-expressing cells after FACS measurements and blue squares % of viable cells after PI exclusion quantification (right Y-axis). Error bars depict the standard deviation of three different experiments. b Partial inhibition of TNF-α-, IL-1β-, or TLR-mediated HIV reactivation by P-TEFb inhibitors. Human hµglia/HIV (HC01) and (HC69), and rat hT-CHME-5/HIV (HC03) and (HC14) microglial cells were untreated (black) or pre-treated with DRB (red; 10 µM) or flavopiridol (blue; 30 nM) for 30 min prior to treatment with TNF-α (30 ng/mL), IL-1β (10 pg/mL), LPS (1 µg/mL), or poly (I:C) (10 µg/mL), as shown in the X-axis, for 16 h prior to quantification of GFP (Y-axis)