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. Author manuscript; available in PMC: 2010 Mar 1.
Published in final edited form as: Br J Haematol. 2009 Jan 12;144(6):848–855. doi: 10.1111/j.1365-2141.2008.07548.x

Fig 2.

Fig 2

Fig 2

(a) SGN-40 mediates ADCC. ADCC was measured using PBMC from normal volunteers and B-CLL cells at 12.5:1, 25:1 and 50:1 effector:target (E:T) ratio in the presence or absence of 10 µg/mL SGN-40, trastuzumab or rituximab. Columns represent the average of triplicate wells and are representative of three independent experiments; bars, SD. The differences observed are significant for the 12.5:1 (p=0.009) and the 50:1 (p=0.01) effectors to target ratios The overall SGN-40 versus trastuzumab mediated ADCC was significantly higher for SGN-40 (n=10 p<0.003). (b, c, d) ADCC mediated by SGN-40 is predominately mediated by NK. (b) ADCC was measured using PBMC, purified NK and purified B cells from CLL patients at 12.5:1 , 25:1 and 50:1 E:T ratio in presence or absence of 10 µg/mL SGN-40 or trastuzumab. Columns, average of triplicate wells and were representative of three independent experiments; bars, standard deviation. (p<0.001 for 12.5:1, p<0.05 for 25:1, p<0.005 for 50:1 effector to target ratio) (N=3). Autologous Natural killer cell derived from CLL patients had significantly increased ADCC against primary CLL when compared to whole PBMC. (c) Resting or (d) IFNγ-activated monocytes were not able to mediate ADCC with SGN-40.