Non-Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

Anti-mouse FcgammaRIV antibody 9E9 also blocks FcgammaRIII in vivo.

Abstract

Monoclonal antibodies (mAbs), such as the anti-CD20 mAb rituximab, have transformed the treatment ofmalignant disease and are now a firstline treatment of many hematologic conditions. Although in many cases their precise mechanism of action is not fully elucidated,where target cell deletion is critical to effective treatment, Fcg receptors (FcgRs) are now accepted to be directly involved.1-3 There are 4 FcgRs in mice and 6 in humans4; debate still exists overwhich FcgRs play the dominant role(s). Early work investigating this used FcgRI- or FcgRIII-deficient mice and/or FcgRIV blockade using the hamster antibody 9E9,5,6 highlighting a critical role for FcgRI and FcgRIV while indicating redundancy for FcgRIII.7 Here, we investigated the role of different activatory FcgRs in the context of anti-CD20 mAb-mediated B-cell depletion.