| First Author | Nemazee DA | Year | 1989 |
| Journal | Nature | Volume | 337 |
| Issue | 6207 | Pages | 562-6 |
| PubMed ID | 2783762 | Mgi Jnum | J:116735 |
| Mgi Id | MGI:3694963 | Doi | 10.1038/337562a0 |
| Citation | Nemazee DA, et al. (1989) Clonal deletion of B lymphocytes in a transgenic mouse bearing anti-MHC class I antibody genes. Nature 337(6207):562-6 |
| abstractText | B lymphocytes can be rendered specifically unresponsive to antigen by experimental manipulation in vivo and in vitro, but it remains unclear whether or not natural tolerance involves B-cell tolerance because B cells are controlled by T lymphocytes, and in their absence respond poorly to antigen (reviewed in ref. 7). In addition, autoantibody-producing cells can be found in normal mice and their formation is enhanced by B-cell mitogens such as lipopolysaccharides. We have studied B-cell tolerance in transgenic mice using genes for IgM anti-H-2k MHC class I antibody. In H-2d transgenic mice about 25-50% of the splenic B cells bear membrane immunoglobulin of this specificity, and abundant serum IgM encoded by the transgenes is produced. In contrast, H-2k x H-2d (H-2-d/k) transgenic mice lack B cells bearing the anti-H-2k idiotype and contain no detectable serum anti-H-2k antibody, suggesting that very large numbers of autospecific B cells can be controlled by clonal deletion. |
