Figure 5
Figure 5. Lenalidomide treatment of allogenic or autologous derived NK cells resulted in enhanced rituximab-mediated ADCC of untreated CLL cells. (A) ADCC was measured using lenalidomide-treated NK cells from normal volunteers and B-CLL cells at 12.5:1, 25:1, and 50:1 E/T in the presence or absence of 10 μg/mL rituximab or trastuzumab. Columns, average of triplicate wells, were representative of 3 independent experiments; bars represent SD. The overall lenalidomide versus vehicle rituximab-mediated ADCC was significantly higher for lenalidomide (P = .009). (B) ADCC was measured using lenalidomide-treated NK and B cells from CLL patients at 12.5:1 and 25:1 E/T in the presence or absence of 10 μg/mL rituximab or trastuzumab. Columns, average of triplicate wells, were representative of 2 independent experiments; bars represent SD (N = 2, P = .02)

Lenalidomide treatment of allogenic or autologous derived NK cells resulted in enhanced rituximab-mediated ADCC of untreated CLL cells. (A) ADCC was measured using lenalidomide-treated NK cells from normal volunteers and B-CLL cells at 12.5:1, 25:1, and 50:1 E/T in the presence or absence of 10 μg/mL rituximab or trastuzumab. Columns, average of triplicate wells, were representative of 3 independent experiments; bars represent SD. The overall lenalidomide versus vehicle rituximab-mediated ADCC was significantly higher for lenalidomide (P = .009). (B) ADCC was measured using lenalidomide-treated NK and B cells from CLL patients at 12.5:1 and 25:1 E/T in the presence or absence of 10 μg/mL rituximab or trastuzumab. Columns, average of triplicate wells, were representative of 2 independent experiments; bars represent SD (N = 2, P = .02)

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