Figure 1. Glyco- or protein-engineered Fc variants optimized for FcγRIII binding mediated enhanced ADCC by MNC, but did not trigger PMN-mediated cytotoxicity. (A, B) ADCC against EGFR-expressing A431 cells was investigated in 3h ⁵¹chromium release assays in the presence of increasing concentrations of (A) protein-engineered or (B) glyco-engineered antibodies. ADCC by MNC was enhanced by protein- or glyco-engineered variants compared with wild type antibody (left panel). PMN triggered significant ADCC with wild type antibody, but were completely ineffective with both types of variants (right panel). Data are presented as mean ± SEM of at least three independent experiments with different donors. * P ≤ 0.05 for wild type vs. engineered antibodies. (C) FcγRIII-engineered antibody mediated tumor cell adhesion by PMN. A431 cell were co-incubated with GM-CSF stimulated PMN from healthy donors at an E:T ratio of 80:1 in the presence or absence of EGFR-targeted antibodies. After 3 h, microscopy was performed at 40x magnification (t = tumor target cells).