FIG 3.

T cell-dependent IL-2 production enhances NK cell activity in HCMV infection. Different effectors, including unfractionated PBMCs (1 × 10⁶), purified NK cells (NK cell percentage × 10⁶), T cell-depleted PBMCs (1 × 10⁶ − T cell percentage × 10⁶), and purified NK cells plus purified T cells (NK cell percentage × 10⁶ + T cell percentage × 10⁶) from the same HCMV-seropositive donor were cocultured with HCMV-infected autologous macrophages (1 × 10⁵) for 48 h, and then activity of NK cells (gated on CD3⁻ CD56⁺ cells under all conditions) was assessed by surface CD107a expression and intracellular IFN-γ production. For IL-2 blocking experiments, purified anti-IL-2 monoclonal antibody and an isotypic antibody control were added at the beginning of coculturing. (A) One representative experiment out of three from HCMV-seropositive donors is shown. (B) Percentages of IFN-γ and CD107a-positive NK cells with IL-2 blocking antibody or isotypic antibody control from another two HCMV-seropositive donors are shown.