ADCC, but not phagocytosis triggered via hFcRI, depends on the presence of CR3 (CD11b/CD18). (A) hFcRI-mediated ADCC is absent in CR3-deficient mice. Whole blood of NTg,CR3⌈+/−(○), Tg,CR3⌈+/− (▪), or Tg,CR3−/− (◂) mice was incubated with⁵¹Cr-labeled SK-BR-3 tumor cells. ⁵¹Cr release from duplicates was quantitated as reflection of tumor cell lysis. *P < .05, **P < .001 versus values of NTg. (B) Binding of neutrophils to A77x520C9 BsAb-opsonized tumor cells is unaffected in CR3-deficient mice. (C) Binding of neutrophils to tumor cells was quantitated on cytospin preparations (binding index = number of granulocytes/100 tumor cells). **P < .001 versus NTg controls. (D) Microscopical analysis of hFc RI phagocytosis. Peritoneal granulocytes of Tg,CR3⌈+/− (left panel) or Tg,CR3−/− (middle panel) were incubated with C. albicans in the presence or absence of BsAb A77xCan. Phagocytic index (phagocytosed C. albicans/100 cells) was determined on cytospins (right panel). **P < .001 versus NTg controls.