Thus, the FcγRIIB-deficient mice on C57Bl/6 background spontaneously develop autoantibodies and an IC-mediated disease [244]; the transgenic restoration of FcγRIIB on B cells in MRL/lpr [245] and in (NZBxNZW) F1 [246] mice reduces the development of lupus like phenotype. This evidence concerns the gene FCGR2B and systemic lupus erythematosus.