Regulation of Anti-DNA B Cells in Recombination-activating Gene-deficient Mice

doi:10.1084/jem.188.7.1247

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J. Exp. Med., Volume 188, Number 7, October 5, 1998 1247-1254

Regulation of Anti-DNA B Cells in Recombination-activating Gene-deficient Mice

By Hui Xu,^* Hui Li,^* Elisabeth Suri-Payer,^* Richard R. Hardy, and Martin Weigert^*

From the ^* Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544; and the Fox Chase Cancer Center, Institute for Cancer Research, Philadelphia, Pennsylvania 19111

Anti-DNA antibodies are regulated in normal individuals but are found in high concentration in the serum of systemic lupuserythematosus (SLE) patients and the MRL lpr/lpr mouse model ofSLE. We previously studied the regulation of anti-double-stranded(ds)DNA and anti-single-stranded (ss)DNA B cells in a nonautoimmunebackground by generating mice carrying immunoglobulin transgenescoding for anti-DNAs derived from MRL lpr/lpr. Anti-dsDNA B cellsundergo receptor editing, but anti-ssDNA B cells seem to be functionallysilenced. Here we have investigated how anti-DNA B cells are regulatedin recombination- activating gene (RAG)-2^/ mice. In this setting, anti-dsDNA B cells are eliminated by apoptosisin the bone marrow and anti-ssDNA B cells are partially activated.

Key words: anti-DNA antibody; B cell deletion; B cell anergy; recombination-activating gene deficiency; apoptosis

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