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Development of Functional B Cells in a Line of SCID Mice with Transgenes Coding for Anti-Double-Stranded DNA Antibody¹

Gayle C. Bosma^*, Jennifer Oshinsky^*, Kerstin Kiefer^*,, Pamela B. Nakajima^*, Deepshika Charan^*, Cecil Congelton^*, Marko Radic and Melvin J. Bosma^2,*

^* Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, PA 19111; Department of Microbiology and Immunology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107; and Department of Molecular Sciences, College of Medicine, University of Tennessee, Memphis, TN 38163

Deletion or inactivation of anti-self (DNA) B cells has been reported in non-autoimmune mice bearing Ig transgenes that code for Abs with specificity for dsDNA or ssDNA. However, we report a case in which anti-dsDNA B cells appear to escape both deletion and inactivation. We show that B cells (B220⁺IgM⁺) can develop in non-autoimmune SCID mice bearing two site-directed transgenes, 3H9(56R) and V8, that together code for an anti-dsDNA Ab. The B cells appear inactive, because the mice (56RV8 SCID mice) generally lack serum Ig. However, 56RV8 SCID mice are able to produce IgG Ab with specificity for dsDNA when they become "leaky" for T cells or are reconstituted with exogenous T cells from B cell-deficient JH^–/– donors. Thus, anti-dsDNA B cells that escape deletion in 56RV8 SCID mice appear fully functional and can differentiate, class switch, and give rise to IgG-producing cells in the presence of T cells and self-Ag.

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