Figure 6
HIV-1 impaired the ability of DCs to activate autologous T-cell responses against SEB. Mature DCs were pulsed with mock or HIV-1BaL, cultured for ∼24 h and thereafter, incubated with mock or 1 ng/mL SEB for 3 h. The cells were washed and cocultured with TN cells with and without STAT3 or P38MAPK inhibitors. The cocultures were restimulated on d 7 with the same DC conditions and harvested on d 8. (A) T-cell proliferation was measured by 3H-thymidine incorporation (n = 9). (B) The gene levels of CTLA-4, PD-1, TRAIL, TIM-3, CD160, LAG3, BLIMP-1, FOXP3 and DTX1 were assessed by qRT-PCR (n = 4). The experiments were normalized, and statistical analysis was performed by one-way ANOVA (Tukey post hoc test). *P < 0.05, **P < 0.005, ***P < 0.001. (C) The protein expression profile on T cells for CTLA-4, PD-1, TRAIL, TIM-3, CD160, BTLA and LAG3 and (D) PD-1 coexpression with CTLA-4, TRAIL, LAG3, TIM-3 and CD160 on T cells were measured by flow cytometry (n = 4: one representative experiment shown). (E, F) Normalized T-cell proliferation after STAT3 (E) and P38 (F) blockade.