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¹ Department of Pathology and Laboratory Medicine, ² Division of Rheumatology, ³ Division of Endocrinology, Diabetes and Metabolism, and ⁴ Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, PA 19104

CORRESPONDENCE Eline T. Luning Prak: luning{at}mail.med.upenn.edu

Continued antibody gene rearrangement, termed receptor editing, is an important mechanism of central B cell tolerance that may be defective in some autoimmune individuals. We describe a quantitative assay for recombining sequence (RS) rearrangement that we use to estimate levels of antibody light chain receptor editing in various B cell populations. RS rearrangement is a recombination of a noncoding gene segment in the antibody light chain locus. RS rearrangement levels are highest in the most highly edited B cells, and are inappropriately low in autoimmune mouse models of systemic lupus erythematosus (SLE) and type 1 diabetes (T1D), including those without overt disease. Low RS rearrangement levels are also observed in human subjects with SLE or T1D.

Abbreviations used: BP-1, BP-1 (aminopeptidase A); Fr., fraction; iRS, intron RS; KDE, deleting element; NOD, nonobese diabetic; NOR, nonobese resistant; PTPN22, protein tyrosine phosphatase nonreceptor 22; RS, recombining sequence; SLE, systemic lupus erythematosis; T1D, type 1 diabetes.

© 2008 Panigrahi et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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