| First Author | Paul E | Year | 2007 |
| Journal | Int Immunol | Volume | 19 |
| Issue | 4 | Pages | 365-73 |
| PubMed ID | 17307801 | Mgi Jnum | J:119987 |
| Mgi Id | MGI:3703653 | Doi | 10.1093/intimm/dxm002 |
| Citation | Paul E, et al. (2007) Follicular exclusion of autoreactive B cells requires Fc{gamma}RIIb. Int Immunol 19(4):365-73 |
| abstractText | In non-autoimmune mice, the 3H9 transgenic Ig heavy chain can pair with endogenous Iglambda1 light chains to generate B cells with specificity for DNA. These autoreactive cells are actively regulated in vivo, as indicated by the exclusion of lambda1 cells from the splenic B cell follicle and the absence of auto-antibody production. To study the role of Fcgamma receptor IIb (FcgammaRIIb) in peripheral B cell tolerance, FcgammaRIIb(-/-) mice were crossed with C57BL/6 mice bearing a site-directed knock-in of the 3H9 transgene. 3H9FcgammaRIIb(-/-) mice become autoreactive, lose the follicular exclusion of anti-DNA B cells and instead have lambda1 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 FcgammaRIIb-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 FcgammaRIIb-dependent regulation is B cell autonomous. |
