Table 1. Current and future therapeutic exploitation of FcγRIIB.

Therapeutic strategy	Clinical effect	Refs
Modulation of FcγRIIB expression on effector cells	IVIG indirectly increases FcγRIIB expression on ‘effector’ cells	138,139
	Infliximab (Remicade; Centocor/Merck) blocks TNF, leading to increased FcγRIIB expression on monocytes	142
Modulation of IgG-binding to FcγRIIB	Decrease in affinity of depleting monoclonal antibodies for FcγRIIB increases efficacy	45,47
Use of FcγRIIB as a direct therapeutic target	Monoclonal antibody directed against FcγRIIB allowing co-crosslinking of FcγRIIB may induce apoptosis of B cells and plasma cells in lymphoma, myeloma or autoimmunity	40,150,151
	A bispecific antibody that binds antigen-specific BCR and FcγRIIB potentially allows targeted inhibition of autoreactive B cells	-
	Therapeutic antibody targeting IgE receptor can inhibit mast cell degranulation and may be useful in the treatment of allergy	152-155
	Soluble FcγRIIB may inhibit immune complex-mediated immune activation and has shown efficacy in a mouse model of SLE	156

BCR, B cell receptor; FcγR, Fc receptor for IgG; IVIG, intravenous immunoglobulin; SLE, systemic lupus erythematosus; TNF, tumour necrosis factor.