Activation of human platelets in PRP via their Fc-receptor by antigen-antibody complexes or immunoglobulin G: Requirement for particle-bound fibrinogen

While latex bearing antigen-antibody complexes or IgG (L-IgG) had no effect on platelets in plasma (PRP),and particles bearing only fibrinogen (L-Fib) caused only platelet aggregation, the presence of fibrinogen on particles bearing antibody or IgG (L-IgG-Fib) enabled them to cause both aggregation and 14C-serotonin release. Both platelet responses were dependent on the concentrations of the proteins used to treat the particles, were inhibited by a range of release inhibitors and were not dependent on complement. Neither F(ab) 2 1, Fc nor Fab fragments could replace IgG. With washed platelets the presence of fibrinogen on L-IgG abolished the lag phase typical of L-IgG-induced aggregation and release. Although IgG fragments could not replace IgG on particles, either Fc or IgG in the platelet suspension inhibited platelet reaction to L-IgG and L-IgG-Fib, indicating participation of the Fc-receptor. It is thus likely that in PRP antigen-antibody complexes or IgG on particles which also bear fibrinogen react with the platelet Fc-receptor and that adsorbed fibrinogen in some way overcomes inhibition by plasma of Fc-receptor expression.