FcγRIIB in autoimmunity and infection: evolutionary and therapeutic implications

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Abstract
Fc receptor IIB for IgG (FcγRIIB) is the only inhibitory Fc receptor, is expressed on many cell types in the immune system and controls humoral responses, pro-inflammatory cytokine release, antigen uptake and presentation, immune complex handling and many other functions. A role for FcγRIIB in controlling B cell tolerance and autoimmunity has been suggested by studies using FcγRIIB-deficient mice and confirmed by in vivo overexpression studies. Spontaneous polymorphic variants alter the expression and/or function of FcγRIIB in both mice and humans, and have been associated with systemic lupus erythematosus (SLE) and other autoimmune diseases. FcγRIIB balances bacterial clearance and the risk of septic shock in mouse models. Genetic studies have shown that an inhibitory, SLE-associated polymorphism of FcγRIIB can protect children from severe malaria, which could drive the high frequency of this polymorphism observed in sub-Saharan Africa and Southeast Asia, and thus begin to explain the increased susceptibility to SLE seen in people of African and Asian ethnicity. The immunosuppressive effect of intravenous immunoglobulin is at least in part dependent on FcγRIIB, and the receptor itself is being investigated as a therapeutic target.

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