IL-2 restores the ability of WAS and XLT NK cells to accumulate F-actin upon their interaction with sensitive targets. (A) Representative example of FACS analysis. F-actin fluorescence intensity in NK cell binders at time 0 (black line) and 30 minutes (green line). (B) Representative example of confocal microscopy analysis showing F-actin redistribution at the contact area of normal, XLT, and WAS NK cells and sensitive targets. NK cells from 4 healthy donors, 4 XLT patients, and 3 WAS patients, treated or not treated with human recombinant IL-2, were allowed to bind to K562 target cells for 15 minutes at 37°C and then were fixed and stained with rhodamine phalloidin. PBS was used as the imaging solution. Phalloidin staining of conjugates and the corresponding bright-field images are shown (original magnification, × 600). Of 100 conjugates analyzed, F-actin accumulation at the contact area was found in 76.5% ± 1.5% of normal NK cell binders, 30.7% ± 4.3% of XLT-NK cell binders (P < .001), and 25% ± 2.1% of WAS NK cell binders (P < .001). Treatment with IL-2 did not change F-actin accumulation in normal NK cell binders (81% ± 2%), whereas it significantly enhanced F-actin accumulation in XLT and WAS NK cell binders 64% ± 5% and 50% ± 4%, respectively (P < .002). P values were calculated comparing the mean percentage of F-actin redistribution in NK cell-target cell conjugates from patients with XLT and WAS with that of control donors or with that of IL-2-treated XLT and WAS NK cells using the Student t test.