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J Exp Med. 2006 Sep 4;203(9):2157-64. Epub 2006 Aug 21.

Selective dysregulation of the FcgammaIIB receptor on memory B cells in SLE.

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  • 1Department of Medicine, Columbia University Medical Center, New York, NY 10032, USA. mcm2123@columbia.edu

Abstract

The inappropriate expansion and activation of autoreactive memory B cells and plasmablasts contributes to loss of self-tolerance in systemic lupus erythematosus (SLE). Defects in the inhibitory Fc receptor, FcgammaRIIB, have been shown to contribute to B cell activation and autoimmunity in several mouse models of SLE. In this paper, we demonstrate that expression of FcgammaRIIB is routinely up-regulated on memory B cells in the peripheral blood of healthy controls, whereas up-regulation of FcgammaRIIB is considerably decreased in memory B cells of SLE patients. This directly correlates with decreased FcgammaRIIB-mediated suppression of B cell receptor-induced calcium (Ca2+) response in those B cells. We also found substantial overrepresentation of African-American patients among those who failed to up-regulate FcgammaRIIB. These results suggest that the inhibitory receptor, FcgammaRIIB, may be impaired at a critical checkpoint in SLE in the regulation of memory B cells; thus, FcgammaRIIB represents a novel target for therapeutic interventions in this disease.

PMID:
16923849
PMCID:
PMC2118390
DOI:
10.1084/jem.20051503
[PubMed - indexed for MEDLINE]
Free PMC Article
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