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.

journal_name

Immunity

journal_title

Immunity

authors

Bolland S,Ravetch JV

doi

10.1016/s1074-7613(00)00027-3

keywords:

subject

Has Abstract

pub_date

2000-08-01 00:00:00

pages

277-85

issue

2

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(00)00027-3

journal_volume

13

pub_type

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