Anti-DNA antibodies, specifically those that stain nuclei in a homogenous nuclear (HN) fashion, are diagnostic of systemic lupus erythematosus (SLE) and the MRL-lpr/lpr SLE murine model. We have used a heavy chain transgene that increases the frequency of anti-HN antibodies to address whether their production in SLE is the consequence of a defect in B cell tolerance. Anti-HN B cells were undetectable in nonautoimmune-prone transgenic mice, but in MRL-lpr/lpr transgenic mice their Ig was evident in the sera and they were readily retrievable as hybridomas. We conclude that nonautoimmune animals actively delete anti-HN-specific B cells, and that MRL-lpr/lpr mice are defective in this process possibly because of the lpr defect in the fas gene.
Breakdown of B cell tolerance in a mouse model of systemic lupus erythematosus.
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J H Roark, C L Kuntz, K A Nguyen, A J Caton, J Erikson; Breakdown of B cell tolerance in a mouse model of systemic lupus erythematosus. . J Exp Med 1 March 1995; 181 (3): 1157–1167. doi: https://doi.org/10.1084/jem.181.3.1157
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