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There is an increasing appreciation of the deleterious effects of antibody and B cells on acute and chronic transplant outcomes. Many effector functions of antibody are mediated by a family of receptors (FcγRs) that are expressed on most immune cells, including neutrophils, natural killer cells, and B cells. Most FcγRs are activating and controlled by a single inhibitory receptor, FcγRIIB (CD32B), which also regulates some aspects of B-cell activation and antibody production. FcγRIIB-deficient mice develop severe chronic arteriopathy in a murine cardiac allograft model. A single nucleotide polymorphism in human FcγRIIB (rs1050501) results in profound receptor dysfunction and is associated with systemic lupus erythematosus. The frequency of this FcγRIIB-I/T232 polymorphism also shows significant racial variation.

Defunctioning Polymorphism in the Immunoglobulin G Inhibitory Receptor (FcγRIIB-T/T232) Does not Impact on Kidney Transplant or Recipient Survival