| First Author | Bolland S | Year | 2000 |
| Journal | Immunity | Volume | 13 |
| Issue | 2 | Pages | 277-85 |
| PubMed ID | 10981970 | Mgi Jnum | J:64152 |
| Mgi Id | MGI:1888803 | Doi | 10.1016/s1074-7613(00)00027-3 |
| Citation | Bolland S, et al. (2000) Spontaneous autoimmune disease in Fc(gamma)RIIB-deficient mice results from strain-specific epistasis. Immunity 13(2):277-85 |
| abstractText | 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. |
