MDCs enhance HIV-1 infection of T cells, whereas PDCs inhibit it. (A, B) Donor-matched MDCs (A) and PDCs (B) from peripheral blood were differently stimulated with maturation-inducing compounds, as indicated on the x-axis. After 24 hours, the DCs were cocultured with HIV-1 and reporter LuSIV cells. HIV-1 infection of these cells results in luciferase production, which was measured after 24 hours (▪). Note the different scales of the graphs. LuSIV cells were also infected in the presence of only supernatant of stimulated DCs (▦). To determine basal luciferase induction by HIV-1 in the absence of DCs or DC supernatant, LuSIV cells were infected with the respective culturing media only (□). *P < .05; **P < .01 compared with culturing medium. (C) Factors secreted by MDCs following T-cell encounter are not responsible for the stimulation of HIV-1 infection. MDCs were cultured in medium only (left), or were matured with either R-848 (middle) or IFNγ plus MF (right), and were subsequently cocultured with CD40L-expressing J558 cells to mimic T-cell encounter. After 24 hours, the supernatant was collected and incubated with LuSIV cells and HIV-1, followed by luciferase measurement one day later. *P < .01; **P < .001 compared with “no DC.” Background luciferase level of LuSIV cells grown without HIV-1 was subtracted from all data. RLU, relative light units. Error bars represent standard deviations.