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The inhibitory Fc receptor for IgG, FcRIIB, is required for the maintenance of peripheral tolerance by virtue of its role in regulating the activation of B cells in the germinal center and the survival of plasma cells. Autoimmune susceptible mouse strains, as well as patients with autoimmune diseases, display reduced expression of FcRIIB on B cells, thus promoting autoimmunity in these populations

RIIB-/- mice spontaneously develop autoantibodies and autoimmune glomerulonephritis in a strain-dependent fashion. C57Bl/6 mice deficient in this inhibitory receptor develop autoantibodies and autoimmune glomerulonephritis, while the same genetic lesion on the Balb/c backgrond does not result in a spontaneous phenotype. The phenotype results from dysregulation of the B cell compartment resulting from loss of this inhibitory pathway. Subsequence studies have defined the genetic contributions of the B6 background that account for this strain difference.

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