Influence of normal IgG and monoclonal IgG1 or IgG2 on platelet response induced by 5B9 with heparin, and relationship with the FcγRIIA H131R polymorphism. Representative aggregation profiles obtained after addition of 5B9 (18 μg/mL) and heparin (0.5 IU/mL) to washed platelets (WP), PRP, and IgG-depleted PRP from homozygous 131HH (A) and 131RR donors (B). Representative aggregation profiles (C-D) and mean lag times (±1 standard error of the mean) (E) obtained after addition of 5B9 (18 μg/mL) and heparin (0.5 IU/mL) with varying concentrations of polyclonal IgG to IgG-depleted PRP from homozygous 131HH (C) and 131RR (D) donors. The Student t test was used to compare the data obtained in the 2 groups of donors. (F) Mean lag times (±1 standard error of the mean) measured after addition of 5B9 (18 μg/mL) and heparin (0.5 IU/mL) with varying concentrations of human monoclonal IgG1 (cetuximab) or IgG2 (panitumumab) to IgG-depleted PRP from homozygous donors FcγRIIA 131RR and 131HH. The Student t test was used to compare the values obtained in the 2 groups of donors; *P < .05 and **P < .01. Inhibition of monoclonal antibody IV.3 binding (expressed in %) on HH and RR platelets by polyclonal IgG (G) and human monoclonal IgG1 or IgG2 (H). The binding of fluorescein isothiocyanate–conjugated IV.3 on platelets from HH and RR donors in the presence of increasing concentrations of polyclonal human IgG or monomeric IgG1 (cetuximab) or IgG2 (panitimumab) was assessed by flow cytometry. The data are representative of flow cytometry analyses performed with 3 different pairs of HH and RR donors.