Spontaneous autoimmune disease in Fc(gamma)RIIB-deficient mice results from strain-specific epistasis
- PMID: 10981970
- DOI: 10.1016/s1074-7613(00)00027-3
Spontaneous autoimmune disease in Fc(gamma)RIIB-deficient mice results from strain-specific epistasis
Abstract
By virtue of its ability to couple the BCR to an inhibitory pathway, FcgammaRIIB can potentially determine the fate of B cells upon IgG immune complex engagement. We now provide evidence for FcgammaRIIB as a component of a peripheral tolerance pathway with the observation that RIIB-/- mice develop autoantibodies and autoimmune glomerulonephritis in a strain-dependent fashion. Transfer of the autoimmune phenotype is associated with the presence of donor RIIB-/- B cells, with the RIIB+/+ myeloid cells primarily derived from the recipient. These results suggest that deficiency of RIIB on B cells leads to autoimmune disease in specific genetic backgrounds, thus identifying it as a susceptibility factor under the influence of epistatic modifiers for the development of autoimmunity.
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