CD16B and CD32A mediate PMN activation and phagocytosis. (A) Phagocytosis. CLL targets were labeled with PKH26 and incubated for 24 hours in the presence or absence of 10 µg/mL of glycoengineered rituximab (GE-RTX) and/or 10 µg/mL of blocking anti-CD16 (a16) or anti-CD32 (a32) Fab fragments. Phagocytosis was measured by flow cytometry. The statistical significance of adding anti-CD16 and/or anti-CD32 Fab fragments with respect to adding CD20 antibody alone is shown. (B-C) PMN activation. CLL targets were opsonized with 10 µg/mL of glycoengineered rituximab antibody and added to whole blood from healthy donors in the presence or absence of 10 µg/mL of anti-CD16 (a16) or anti-CD32 (a32) F(ab’)2 fragments. CD62L down-modulation on PMNs was measured at 6 hours (panel B), whereas CD11b induction was measured at 24 hours (panel C). The statistical significance of treated vs control (CTRL) samples is shown. All data are the means and standard deviations of 3 independent experiments.
