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.
journal_name
Immunityjournal_title
Immunityauthors
Bolland S,Ravetch JVdoi
10.1016/s1074-7613(00)00027-3keywords:
subject
Has Abstractpub_date
2000-08-01 00:00:00pages
277-85issue
2eissn
1074-7613issn
1097-4180pii
S1074-7613(00)00027-3journal_volume
13pub_type
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