Trogocytosis of B-cell surface proteins to effector cells. Daudi cells were mixed with purified monocytes 1:1 (A-C), PBMCs 1:5 (D), monocyte-depleted PBMCs 1:5 (E), or purified granulocytes 1:2 (F-G) and treated for 1 hour with epratuzumab (red dots) or labetuzumab (blue dots) before analysis by flow cytometry. Monocyte, lymphocyte, granulocyte, and Daudi populations were first gated by FSC vs SSC. The monocyte gate (A) was further separated into CD14⁺⁺CD16^– (B) and CD14⁺CD16⁺ (C) monocyte populations, with each evaluated for CD19 and CD22 levels. CD14^–CD16⁺ cells were isolated from the lymphocyte gate (NK cell phenotype) of complete PBMCs (D) or monocyte-depleted PBMCs (E) and evaluated for CD19 and CD22 levels. The granulocyte gate was further refined for CD16⁺ cells and evaluated for CD19 (F-G), CD22 (F), and CD79b (G). Representative dot plots obtained from triplicate analyses are shown. The Daudi cells (CD19⁺ cells in the Daudi gate) were analyzed for CD19 and CD22 levels following epratuzumab treatment with PBMCs, purified monocytes, or monocyte-depleted PBMCs (H), or purified granulocytes (I), and graphed as the % MFI of the isotype control treatment. (J-K) The levels of CD22 (J) and CD19 (K) on monocytes (solid line) and Daudi cells (dashed line) were measured over a 20-hour treatment with epratuzumab (blue line) or isotype control (red line). Each sample was evaluated in triplicate. Error bars represent SD.