CD37-SMIP induced ADCC but not CDC in primary CLL B cells. (A) CD37-SMIP induced ADCC against CLL B cells. Ability of trastuzumab, CD37-SMIP, alemtuzumab, or rituximab to mediate ADCC was evaluated using fresh human PBMC as effector cells and CD19⁺ primary CLL B cells as target cells at the indicated effector/target (E:T) ratios. Data shown here are summary of 6 patient samples and error bars represent SD among patients. (B) CD37 SMIP does not mediate CDC. Primary CLL B cells were treated with media, trastuzumab, CD37-SMIP, or alemtuzumab in the presence of media, human plasma or heat-inactivated human plasma for 1 hour. The CDC function was evaluated by propidium iodide staining. Summary of the results from 4 CLL patient samples are shown. Error bars show SD among patients. (C) In vitro evaluation of CD37-SMIP–induced ADCC function by NK cells, monocytes, or PBMC effector cells. Effect of purified NK cells, monocytes, or PBMC effector cells to mediate CD37-SMIP-, trastuzumab-, or alemtuzumab-dependent ADCC function against CD19⁺ primary CLL B cells as target cells was evaluated at the indicated effector/target (E:T) ratios by standard chromium release assay as described under “Materials and methods.” Data shown here are the summary of results from 6 patient samples, and error bars represent SD among patients. (D) Naive or IFN-γ activated monocytes failed to mediate CD37-SMIP–dependent ADCC function against CLL B cell targets. The effects of CD37-SMIP–induced ADCC using naive or IFN-γ–activated monocytes were measured as described above. Data shown here are summary of 3 patient samples (± SD).