Abstract
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease of uncertain etiology that is influenced by both genetic and environmental factors. Although lupus is usually considered to be primarily a genetic disorder, environmental triggers, such as ultraviolet light and certain medications (1), can trigger the disease in genetically susceptible hosts. The isoprenoid alkane pristane (2,6,10,14-tetramethypentadecane), a component of mineral oil, has recently been shown to be a powerful environmental trigger that induces a lupus-like syndrome in nonautoimmune strains of mice (2,3). Pristane-treated mice develop autoantibodies associated with SLE, including the marker antibodies anti-Sm, double-stranded DNA (dsDNA), and ribosomal P, as well as less disease-specific autoantibodies (anti-nRNP, Su, single-stranded DNA [ssDANA], and histone) at titers as high as 1:250,000 (4). They also develop immune complex—mediated glomerulonephritis closely resembling human lupus nephritis with glomerular IgG, IgM and complement deposition, and mesangial hypercellularity (2,3). These similarities with human lupus and the fact that disease can be induced in virtually all normal strains of mice, regardless of genetic background, suggest that this new inducible lupus model may be useful for defining the immunologic defects causing SLE.
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Satoh, M., Richards, H.B., Reeves, W.H. (1999). Pathogenesis of Autoantibody Production and Glomerulonephritis in Pristane-Treated Mice. In: Kammer, G.M., Tsokos, G.C. (eds) Lupus. Contemporary Immunology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-703-1_25
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DOI: https://doi.org/10.1007/978-1-59259-703-1_25
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