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Publication : Arteritis in a novel congenic strain of mice derived from MRL/Lpr lupus mice: genetic dissociation from glomerulonephritis and limited autoantibody production.

First Author  Nose M Year  1996
Journal  Am J Pathol Volume  149
Issue  5 Pages  1763-9
PubMed ID  8909264 Mgi Jnum  J:36611
Mgi Id  MGI:84038 Citation  Nose M, et al. (1996) Arteritis in a novel congenic strain of mice derived from MRL/Lpr lupus mice: genetic dissociation from glomerulonephritis and limited autoantibody production. Am J Pathol 149(5):1763-9
abstractText  An MRL/Mp strain of mice bearing the Fas deletion mutant gene, lpr (MRL/lpr), spontaneously develop systemic vasculitis and glomerulonephritis in the same individual, and both have been thought to be associated with an increase in circulating immune complexes and autoantibodies. However, the genetic basis of these diseases is poorly understood. A novel recombinant congenic mouse strain, McH5-lpr/lpr, which was established by rearrangement of the genetic background of MRL/lpr mice by hybridization with C3H/HeJ-lpr/lpr mice, developed severe granulomatous polyarteritis, as did the MRL/lpr strain, but not glomerulonephritis. Serum levels of anti- DNA and anti-myeloperoxidase antibodies in these mice were significantly reduced, as compared with MRL/lpr mice, although rheumatoid factors were not. These results indicate that each of these two disease, arteritis and glomerulonephritis, is under the control of different background gene(s), suggesting a different pathological basis of these diseases, and that anti-DNA and anti- myeloperoxidase autoantibodies appear to have a limited pathogenic role in granulomatous arteritis in the mouse strain described.
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