Vpu Exploits the Cross-Talk between BST2 and the ILT7 Receptor to Suppress Anti-HIV-1 Responses by Plasmacytoid Dendritic Cells
Fig 5
BST2 at the surface of infected cells is required for Vpu-mediated control of IFN-I production.
MT4 cells were mock-infected or infected with GFP-marked NL4.3 WT or dU viruses and pre-incubated with anti-BST2 rabbit polyclonal (Rb BST2 Ab) or pre-immune (Rb PI) Abs or left untreated (No Ab). (A) Mock cells were subsequently stained for surface BST2 using mAb 26F8 and analyzed by flow cytometry. As a positive control, cells were directly stained with mAb 26F8. (B-C) The indicated MT4 cells were co-cultured with PBMCs. After 24 h, levels of IFN-I released in supernatants were measured. A representative example of absolute levels (B) or relative percentages (C) of IFN-I produced after co-culture of PBMCs with infected MT4 cells pre-treated with the indicated Abs are shown. The amount of IFN-I released by PBMCs in contact with dU HIV-infected cells in presence of Rb PI was set at 100% (n = 4). Two-tailed paired t-test was used (** p<0.01, * p<0.05, ns not significant (p>0.05)). Error bars represent SD.