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7
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Data presented in this report demonstrate that susceptibility to lupus nephritis is impacted by allele-specific genetic interactions between genes enhancing and suppressing disease
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Morel L., Tian X-H., Croker B.P., Wakeland E.K. Epistatic modifiers of autoimmunity in a murine model of lupus nephritis. Immunity. 11:1999;131-139. Data presented in this report demonstrate that susceptibility to lupus nephritis is impacted by allele-specific genetic interactions between genes enhancing and suppressing disease.
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11
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Hogarth M.B., Slingsby J.H., Allen P.J., Thompson E.M., Chandler P., Davies K.A., Simpson E., Morley B.J., Walport M.J. Multiple lupus susceptibility loci map to chromosome 1 in BXSB mice. J Immunol. 161:1998;2753-2761.
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13
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Linkage of a major quantitative trait locus to Yaa gene-induced lupus-like nephritis in (NZW x C57BL/6)F1 mice
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Santiago M.L., Mary C., Parzy D., Jacquet C., Montagutelli X., Parkhouse R.M., Lemoine R., Izui S., Reininger L. Linkage of a major quantitative trait locus to Yaa gene-induced lupus-like nephritis in (NZW x C57BL/6)F1 mice. Eur J Immunol. 28:1998;4257-4267.
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14
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Ida A., Hirose S., Hamano Y., Kodera S., Jiang Y., Abe M., Zhang D., Nishimura H., Shirai T. Multigenic control of lupus-associated antiphospholipid syndrome in a model of (NZW x BXSB) F1 mice. Eur J Immunol. 28:1998;2694-2703.
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15
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This study presents data demonstrating that fatal lupus nephritis can be produced in normal B6 mice by the introduction of Sle1 and Sle3 from the NZM2410 lupus-prone mouse strain
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Mohan C., Morel L., Yang P., Watanabe H., Croker B.P., Gilkeson G.S., Wakeland E.K. Genetic dissection of lupus pathogenesis: a recipe for nephrophilic autoantibodies. J Clin Invest. 103:1999;1685-1695. This study presents data demonstrating that fatal lupus nephritis can be produced in normal B6 mice by the introduction of Sle1 and Sle3 from the NZM2410 lupus-prone mouse strain.
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Mohan C., Alas E., Morel L., Yang P., Wakeland E.K. Genetic dissection of SLE pathogenesis: Sle1 on murine chromosome 1 leads to a selective loss of tolerance to H2A/H2B/DNA subnucelosomes. J Clin Invest. 101:1998;1362-1372.
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Botto M., Dell'Agnola C., Bygrave A.E., Thompson E.M., Cook H.T., Petry F., Loos M., Pandolfi P.P., Walport M.J. Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies. Nat Genet. 19:1998;56-59. This study presents results demonstrating that C1q deficiencies mediate a loss in tolerance to chromatin antigens and lead to an increase in apoptotic cell bodies in diseased kidneys.
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This study demonstrates the effect of deficiencies in Sap on immune tolerance to chromatin and demonstrates that Sap deficiency impacts the clearance of chromatin in vivo
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