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Resistance is futile: Targeting the inhibitory FcγRIIB (CD32B) to maximize immunotherapy
Ali Roghanian1, Mark S Cragg2, Björn Frendéus3
1Antibody & Vaccine Group, Cancer Sciences Unit, Faculty of Medicine, University of Southampton, Southampton General Hospital, Southampton, UK; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, USA.
Monoclonal antibodies (mAb) are central to the treatment of several types of malignancy. However, these reagents are subject to particular types of resistance. Several resistance mechanisms are regulated by the inhibitory FcγRIIB. We recently developed mAbs to block FcγRIIB and provided in vivo proof-of-concept for their ability to overcome FcγRIIB-mediated resistance.
Monoclonal antibodies (mAb) are central to the treatment of several types of malignancy. However, these reagents are subject to particular types of resistance. Several resistance mechanisms are regulated by the inhibitory FcγRIIB. We recently developed mAbs to block FcγRIIB and provided in vivo proof-of-concept for their ability to overcome FcγRIIB-mediated resistance.
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