Figure 3
Figure 3. Direct role of activating receptors in CIK-mediated lysis of tumor targets. (A-B) RAJI (A) and MOLT4 (B) cells were analyzed for expression of MICA/B and ULBP-1, -2, and -3 (NKG2D ligands), and PVR and Nectin-2 (DNAM-1 ligands) by flow cytometry. Gray profiles represent isotype control. (C-D) Blocking of activating receptors NKG2D, NKp30, and DNAM-1 in CIK cells cytotoxicity against RAJI (C) and MOLT4 (D) targets. CIK cells were preincubated with saturating concentrations of anti-NKG2D, anti-NKp30, anti–DNAM-1, and cytotoxic activity was measured in calcein-release assays. The data were mean ± SD obtained from 3 independent experiments and were analyzed by Student t test, *P < .05, compared with control in the absence of mAbs.

Direct role of activating receptors in CIK-mediated lysis of tumor targets. (A-B) RAJI (A) and MOLT4 (B) cells were analyzed for expression of MICA/B and ULBP-1, -2, and -3 (NKG2D ligands), and PVR and Nectin-2 (DNAM-1 ligands) by flow cytometry. Gray profiles represent isotype control. (C-D) Blocking of activating receptors NKG2D, NKp30, and DNAM-1 in CIK cells cytotoxicity against RAJI (C) and MOLT4 (D) targets. CIK cells were preincubated with saturating concentrations of anti-NKG2D, anti-NKp30, anti–DNAM-1, and cytotoxic activity was measured in calcein-release assays. The data were mean ± SD obtained from 3 independent experiments and were analyzed by Student t test, *P < .05, compared with control in the absence of mAbs.

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