| First Author | O'Keefe TL | Year | 1999 |
| Journal | J Exp Med | Volume | 189 |
| Issue | 8 | Pages | 1307-13 |
| PubMed ID | 10209047 | Mgi Jnum | J:76975 |
| Mgi Id | MGI:2180694 | Doi | 10.1084/jem.189.8.1307 |
| Citation | O'Keefe TL, et al. (1999) Deficiency in CD22, a B cell-specific inhibitory receptor, is sufficient to predispose to development of high affinity autoantibodies. J Exp Med 189(8):1307-13 |
| abstractText | CD22 is a B cell-specific transmembrane glycoprotein that acts to dampen signals generated through the B cell antigen receptor (BCR): B cells from CD22-deficient mice give increased Ca2+ fluxes on BCR ligation. Here we show that this B cell hyperresponsiveness correlates with the development of autoantibodies. After the age of eight months, CD22-deficient mice developed high titers of serum IgG directed against double-stranded DNA; these antibodies were of multiclonal origin, somatically mutated, and high affinity. Increased titers of antibodies to cardiolipin and myeloperoxidase were also noted. The results demonstrate that a single gene defect exclusive to B lymphocytes is, without additional contrivance, sufficient to trigger autoantibody development in a large proportion of aging animals. Thus, CD22 might have evolved specifically to regulate B cell triggering thresholds for the avoidance of autoimmunity. |
