Biological functions triggered via FcRI on transgenic neutrophils. (A) Phagocytosis of BsAb-coated OE by granulocytes of nontransgenic (upper left panel) and transgenic (upper right panel) mice analyzed by microscopy. Flow cytometric analysis is shown in lower panels. White blood cells were incubated with nonopsonized OE-FITC (thin lines) or A77xOE BsAb opsonized OE-FITC (bold lines). Nonphagocytosed OE were lysed. FITC-fluorescence of granulocytes reflects phagocytosed OE. Gr-1-PE was used to identify granulocytes. (B) Microscopic analysis of phagocytosis of BsAb-coated C. albicans by granulocytes of nontransgenic (left panel) or transgenic (right panel) mice. (C) C. albicans killing by PMN from transgenic and nontransgenic mice in the presence of medium alone (white bars) or 10 μg/mL BsAb A77xCan (black bars). *P < .05 versus NTg control. (D) Capacity of FcRI to trigger whole blood ADCC. Whole blood of NTg (○) and Tg (▪) mice was incubated with⁵¹Cr-labeled SK-BR-3 tumor cells in the presence of hFc RI-directed BsAb. ⁵¹Cr release from duplicates was measured. *P < .05 versus values of NTg. The data shown (mean ± standard deviation [SD]) are representative of results obtained in four separate experiments.