Skip to main content
. 2002 Aug;129(2):265–271. doi: 10.1046/j.1365-2249.2002.01919.x

Fig. 2.

Fig. 2

Fig. 2

Fig. 2

NK-92 ci utilizes both perforin dependent and independent killing mechanisms. (a) Target cells, Jurkat and K562, were incubated with either untreated NK-92 ci (▪), CMA treated NK-92 ci (▪) or NK-92 ci in the presence of EGTA (□), in a 5-h CRA at an E:T ratio of 10:1. (b) NK-92 ci killing induces Annexin V binding to target cells. Jurkat and K562 cells were incubated either alone (upper panels) or with CMA treated NK-92 ci cells (lower panels) for 4 h prior to labelling with Annexin V-FITC. NK-92 ci cells were gated out on the basis of CD56 staining. (c) CD95 blocking antibody partially inhibits apoptotic killing. Jurkat cells were incubated with CMA treated NK-92 in the presence or absence or 2 μg/ml ZB4 antibody. Chromium release was measured after a 6-h CRA. The results shown are the averages ± SE of 6 experiments.