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. 2006 Apr 20;103(18):7012–7017. doi: 10.1073/pnas.0601851103

Fig. 2.

Fig. 2.

Deficient cytokine and chemokine production in response to ITAM signaling by CD45−/− NK cells. WT and CD45−/− NK cells were incubated on plate-bound mAbs for NKG2D and Ly49D (Left) or NK1.1 and mouse IgG2a (a natural ligand of CD16) (Right). C, control mAb. Supernatants were harvested at 16 h and assayed for IFNγ (A) or MIP-1β (Β) by ELISA. All mAb stimulation was performed in the presence of soluble anti-CD16/32 mAb (2.4G2) to block Fc receptor activation, except in experiments in which NK cells were stimulated via CD16 by plate-bound mouse IgG2a. (C) IFNγ (Left) and MIP-1β (Right) secretion after PMA (25 ng/ml) and ionomycin (1 μg/ml) stimulation. Results are representative of two to five independent experiments.