| First Author | Makdasi E | Year | 2009 |
| Journal | J Immunol | Volume | 182 |
| Issue | 10 | Pages | 6143-8 |
| PubMed ID | 19414767 | Mgi Jnum | J:150296 |
| Mgi Id | MGI:3850287 | Doi | 10.4049/jimmunol.0803610 |
| Citation | Makdasi E, et al. (2009) Autoreactive anti-DNA transgenic B cells in lupus-prone New Zealand black/New Zealand white mice show near perfect L chain allelic exclusion. J Immunol 182(10):6143-8 |
| abstractText | Recent work on B cell tolerance and autoimmunity has suggested the L chain allelic inclusion is a property of autoreactive B cells and is closely linked to receptor editing. Allelic inclusion could rescue autoreactive B cells from clonal deletion by reducing their effective BCR surface density. We have investigated this phenomenon in anti-DNA producing hybridomas, derived from different strains of Ig gene-targeted, lupus-prone NZB/NZW mice. Our results indicate that isotype and allelic exclusion was strictly maintained in most high- and low-affinity, edited and nonedited, anti-DNA transgenic B cells. However, a substantial fraction of the anti-DNA hybridomas expressed a very restricted set of nonproductively rearranged L chain mRNA, in addition to the productive anti-DNA L chain. The aberrant L chains could have a role in the selection and survival of autoreactive B cells in these autoimmune mice. |
