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International Immunology Advance Access originally published online on February 16, 2007
International Immunology 2007 19(4):365-373; doi:10.1093/intimm/dxm002
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Follicular exclusion of autoreactive B cells requires Fc{gamma}RIIb

Elahna Paul1,2,*, Annette Nelde3,4,*, Admar Verschoor3,4 and Michael C. Carroll1,3,4

1 Department of Pediatrics, Harvard Medical School, Boston, MA, USA
2 Division of Pediatric Nephrology, Massachusetts General Hospital, Boston, MA, USA
3 Department of Pathology, Harvard Medical School, Boston, MA, USA
4 CBR Institute for Biomedical Research, Boston, MA, USA

Correspondence to: E. Paul; E-mail: epaul{at}partners.org

In non-autoimmune mice, the 3H9 transgenic Ig heavy chain can pair with endogenous Ig{lambda}1 light chains to generate B cells with specificity for DNA. These autoreactive cells are actively regulated in vivo, as indicated by the exclusion of {lambda}1 cells from the splenic B cell follicle and the absence of auto-antibody production. To study the role of Fc{gamma} receptor IIb (Fc{gamma}RIIb) in peripheral B cell tolerance, Fc{gamma}RIIb–/– mice were crossed with C57BL/6 mice bearing a site-directed knock-in of the 3H9 transgene. 3H9Fc{gamma}RIIb–/– mice become autoreactive, lose the follicular exclusion of anti-DNA B cells and instead have {lambda}1 B cells located within splenic germinal centers. They have increased frequencies of splenic auto-antibody-producing cells and elevated titers of IgG anti-DNA auto-antibody. The data implicate an Fc{gamma}RIIb-dependent checkpoint that can exclude autoreactive B cells from splenic follicles. By restricting their participation in germinal center reactions, this putative checkpoint helps attenuate the production of potentially pathogenic auto-antibodies. The data further suggest that this Fc{gamma}RIIb-dependent regulation is B cell autonomous.

Keywords: autoimmunity, Fc receptors, lupus, rodent, tolerance

* These authors contributed equally to this work.

Transmitting editor: R. S. Geha

Received 12 August 2006, accepted 9 January 2007.


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