Anti-DNA antibodies are regulated in normal individuals but are found in high concentration in the serum of systemic lupus erythematosus (SLE) patients and the MRL lpr/lpr mouse model of SLE. We previously studied the regulation of anti–double-stranded (ds)DNA and anti–single-stranded (ss)DNA B cells in a nonautoimmune background by generating mice carrying immunoglobulin transgenes coding for anti-DNAs derived from MRL lpr/lpr. Anti-dsDNA B cells undergo receptor editing, but anti-ssDNA B cells seem to be functionally silenced. Here we have investigated how anti-DNA B cells are regulated in recombination- activating gene (RAG)-2−/− mice. In this setting, anti-dsDNA B cells are eliminated by apoptosis in the bone marrow and anti-ssDNA B cells are partially activated.
Regulation of Anti-DNA B Cells in Recombination-activating Gene–deficient Mice
Address correspondence to Martin Weigert, Princeton University, Department of Molecular Biology, 401 Schultz Laboratory, Washington Rd., Princeton, NJ 08544. Phone: 609-258-4698; Fax: 609-258-2205; E-mail: [email protected]
Dedicated to the memory of Eugenia Spanopoulou, whose work (described in reference 17) was the forerunner of this article.
Martin Weigert is a recipient of a National Institutes of Health grant (GM-20964-24) and Elisabeth Suri-Payer is supported by an Arthritis Investigator Award from the Arthritis Foundation.
Hui Xu, Hui Li, Elisabeth Suri-Payer, Richard R. Hardy, Martin Weigert; Regulation of Anti-DNA B Cells in Recombination-activating Gene–deficient Mice . J Exp Med 5 October 1998; 188 (7): 1247–1254. doi: https://doi.org/10.1084/jem.188.7.1247
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