Involvement of CD11b/CD18 in enhanced neutrophil adhesion by Fcγ receptor stimulation

Neutrophils showed a rapid and transient adhesion to immunoglobulin G (IgG)-coated plates com- pared with their adhesion to bovine serum albumin (BSA)-coated plates: the adhesion reached a peak after 15 mm of incubation and then gradually returned to almost the basal state in 60 mm. The addition of monomeric IgG or anti-Fc-yRII monoclonal antibody (mAb) (IV.3) sup- pressed the increase in adhesion, whereas anti-Fc'yRIII mAb (3G8) was hardly effective, indicating that the inter- action of Fc'yR, especially Fc-yRII, with coated IgG is in- volved in the process. Adhesion was also blocked by cytochalasin B, suggesting that functional actin filament structures are crucial. Protein kinase inhibitors, erbstatin and genistein, inhibited the adhesion in a dose-dependent manner. The adhesion was inhibited by anti-CD11b (M1/70) and anti-CD18 (MHM23, TS1i18) mAbs. Moreover, neutrophils from a patient with complete leu- kocyte adhesion deficiency syndrome did not show in- creased adhesion to IgG-coated plates. The adhesion of neutrophils to fibrinogen- and BSA-coated plates was also increased when FcyR was stimulated in the fluid phase with soluble aggregated IgG, which was also inhibited by anti-CD11b mAb. Stimulation of neutrophil FcyR with soluble aggregated IgG enhanced the expression of CD11b in concert with the enhanced adhesion. These data collec- tively suggest that stimulation via Fc-yR evokes a tyrosine kinase-dependent and actin filament-dependent in-