The Journal of Experimental Medicine
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Published online January 8, 2007
doi:10.1084/jem.20061918
The Journal of Experimental Medicine, Vol. 204, No. 1, 153-160
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Casellas et al.
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ARTICLE

 Ig{kappa} allelic inclusion is a consequence of receptor editing

Rafael Casellas1, Qingzhao Zhang2,3, Nai-Ying Zheng2, Melissa D. Mathias2, Kenneth Smith2, and Patrick C. Wilson2,3,4

1 Genomic Integrity and Immunity, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892
2 Molecular Immunogenetics Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104
3 Department of Pathology and 4 Department of Microbiology and Immunology, Oklahoma University of Health Sciences, Oklahoma City, OK 73104

CORRESPONDENCE Patrick C. Wilson: wilsonp{at}omrf.ouhsc.edu

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 Ig{kappa} 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.

Abbreviations used: ANA, antinuclear antigen; hC{kappa}, human {kappa} constant region; HRP, horse-radish peroxidase; mC{kappa}, mouse {kappa} constant region; MZ, marginal zone; OOF, out-of-frame; YFP, yellow fluorescent protein.

R. Casellas and Q. Zhang contributed equally to this paper.


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