Igκ allelic inclusion is a consequence of receptor editing
Open Access
- 8 January 2007
- journal article
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 204 (1) , 153-160
- https://doi.org/10.1084/jem.20061918
Abstract
The discovery of lymphocytes bearing two light chains in mice carrying self-reactive antibody transgenes has challenged the "one lymphocyte-one antibody" rule. However, the extent and nature of allelically included cells in normal mice is unknown. We show that 10% of mature B cells coexpress both Igkappa alleles. These cells are not the result of failure in allelic exclusion per se, but arise through receptor editing. We find that under physiological conditions, editing occurs both by deletion and by inclusion with equal probability. In addition, we demonstrate that B lymphocytes carrying two B-cell receptors are recruited to germinal center reactions, and thus fully participate in humoral immune responses. Our data measure the scope of allelic inclusion and provide a mechanism whereby autoreactive B cells might "escape" central tolerance.Keywords
This publication has 36 references indexed in Scilit:
- A stepwise epigenetic process controls immunoglobulin allelic exclusionNature Reviews Immunology, 2004
- Human Autoantibody Silencing by Immunoglobulin Light ChainsThe Journal of Experimental Medicine, 2004
- Variegated Transcriptional Activation of the Immunoglobulin κ Locus in Pre-B Cells Contributes to the Allelic Exclusion of Light-Chain ExpressionCell, 2004
- OcaB Is Required for Normal Transcription and V(D)J Recombination of a Subset of Immunoglobulin κ GenesCell, 2002
- Contribution of Receptor Editing to the Antibody RepertoireScience, 2001
- Revising B Cell ReceptorsThe Journal of Experimental Medicine, 2000
- Frequencies of Multiple IgL Chain Gene Rearrangements in Single Normal or κL Chain–Deficient B Lineage CellsImmunity, 1999
- Receptor editing: an approach by autoreactive B cells to escape tolerance.The Journal of Experimental Medicine, 1993
- A transgenic model of autoimmune hemolytic anemia.The Journal of Experimental Medicine, 1992
- Somatic generation of antibody diversityNature, 1983