Schematic model for the role of Mac-1 in FcR-mediated PMN cytotoxicity.

(A) Recognition and binding of PMNs (Mac-1^+/− and Mac-1^−/−) to Ab-coated tumor targets initiated via FcRs. (B) PMN spreading onto tumor targets proceeded by immunologic synapse formation is dependent on Mac-1. This is accompanied by reorganization of the actin cytoskeleton. (C) Both Mac-1^+/− and Mac-1^−/− PMNs become activated, resulting in mobilization of specific granules and respiratory burst activity. Mac-1^−/− PMNs are, however, unable to release toxic agents in close proximity of tumor targets, resulting in defective cytolysis.