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Background  The significance of a unique inhibitory Fc receptor for IgG, FcγRIIB (RIIB), in the prevention of spontaneous production of autoantibodies remains controversial, due mainly to the fact that the  RIIB  locus is adjacent to the autoimmune-related  SLAM  locus harboring the genes coding for signaling lymphocyte activation molecules, making it difficult to isolate the effect of RIIB deletion from that of  SLAM  in gene-targeted mice. Our objective was to determine the influence of  RIIB  deletion on the spontaneous development of autoimmune diseases and to compare it with that of potentially pathogenic  SLAM .    Results  We established two congenic C57BL/6 (B6) strains, one with the  RIIB  deletion and the other with  SLAM , by backcrossing 129/SvJ-based  RIIB -deficient mice into the B6 genetic background extensively. The RIIB deficiency indeed led to the production and/or accumulation of a small amount of anti-nuclear autoantibodies (ANAs) and to weak IgG immune-complex deposition in glomeruli without any obvious manifestation of lupus nephritis. In contrast, pathogenic  SLAM  in the B6 genetic background induced ANAs but no IgG immune-complex deposition in the kidneys. Naïve  SLAM  mice but not RIIB-deficient mice exhibited hyperplasia of splenic germinal centers.    Conclusion  The present results clarify the roles of RIIB in preventing production and/or accumulation of a small amount of ANAs, and development of glomerulonephritis. The combined effects of RIIB deletion and pathogenic SLAM can lead to severe lupus nephritis in the B6 genetic background.    Electronic supplementary material  The online version of this article (doi:10.1186/s12865-014-0047-y) contains supplementary material, which is available to authorized users.

bmc immunology

Dichotomy in FcγRIIB deficiency and autoimmune-prone SLAM haplotype clarifies the roles of the Fc receptor in development of autoantibodies and glomerulonephritis