| First Author | Yarkoni Y | Year | 2006 |
| Journal | Eur J Immunol | Volume | 36 |
| Issue | 10 | Pages | 2755-67 |
| PubMed ID | 16983722 | Mgi Jnum | J:118137 |
| Mgi Id | MGI:3698668 | Doi | 10.1002/eji.200636190 |
| Citation | Yarkoni Y, et al. (2006) Peripheral B cell receptor editing may promote the production of high-affinity autoantibodies in CD22-deficient mice. Eur J Immunol 36(10):2755-67 |
| abstractText | CD22-deficient mice are characterized by B cell hyperactivity and autoimmunity. We have constructed knock-in CD22-/- mice, expressing an anti-DNA heavy (H) chain (D42), alone or combined with Vkappa1-Jkappa1 or Vkappa8-Jkappa5 light (L) chains. The Ig-targeted mice produced a lupus-like serology that was age- and sex-dependent. High-affinity IgG autoantibodies were largely dependent on the selection of B cells with a particular H/L combination, in which a non-transgenic, endogenous L chain was assembled by secondary rearrangements through the mechanism of receptor editing. Moreover, we present evidence that these secondary rearrangements are very prominent in splenic peripheral B cells. Since CD22 is primarily expressed on the surface of peripheral B cells, we propose a model for the development of a lupus-like autoimmune disease by a combination of peripheral receptor editing and abnormal B cell activation. |
