Fig. 6.

IPP-expanded Vγ9Vδ2 T cells inhibit pandemic H1N1 virus replication in both a cytotoxic and noncytolytic manner. (A) MDMs (target) were infected by mock or pdmH1N1 virus at an MOI of 2 for 1 h and then cocultured with purified IPP-expanded Vγ9Vδ2 T cells (effector) at indicated effector/target (E/T) ratios (range, 0:1 to 20:1) for 6 h. The percentages (means ± SEM) of dead MDMs among whole target cells (CD3⁻ population) identified as CD3⁻ EthD-2⁺ from four separate experiments are shown. (B) MDMs were infected with pdmH1N1 virus at an MOI of 2 and cultured alone or with Vγ9Vδ2 T cells at an E/T ratio of 10:1 for 48 h. Total RNA was extracted from both cells and supernatant, and viral matrix gene copies were quantified by real-time RT-PCR, as described in Materials and Methods. Data are means ± SEM for viral M1 gene copies per 10⁵ MDMs from four separate experiments. (C) A549 cells (target) in the bottom wells were infected with pdmH1N1 virus at an MOI of 2 for 1 h. Then, purified Vγ9Vδ2 T cells (effector) were added into transwell inserts at an E/T ratio of 5:1. IPP (6 μg/ml) was added alone or together with anti-IFN-γ MAb (αIFN-γ; 10 μg/ml) or goat IgG (gIgG; 10 μg/ml). The A549 cells were collected at day 4 postinfection. Viral copies were quantified by real-time PCR. Data are shown as means ± standard error for viral M1 gene copies per 10⁴ copies of β-actin from four separate experiments. *, P < 0.05.