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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

An autosomal recessive gene that delays expression of lupus in BXSB mice.

We report the generation and serologic, cellular, histologic, and genetic characteristics of a BXSB/MpJScr substrain, termed BXSB/MpJScr-ll/ll, that has lost early-life male lupus disease. Classic genetic analysis suggested that delayed disease expression results from the action of a single autosomal recessive gene. This putative gene, referred to as ll (long-lived), causes a significant delay in expression of autoimmune serology (total serum IgG and anti-nuclear antibodies levels), monocytosis, and of immune complex-mediated histopathologic changes such as glomerulonephritis, arteritis, and myocardial infarction. Presumably as a consequence of the delayed immunopathology male BXSB/MpJScr-ll/ll mice live three to four times longer than regular BXSB/MpJScr. This strain might be useful for analysis of single genes responsible for severe autoimmune disease expression.[1]


  1. An autosomal recessive gene that delays expression of lupus in BXSB mice. Kofler, R., McConahey, P.J., Duchosal, M.A., Balderas, R.S., Theofilopoulos, A.N., Dixon, F.J. J. Immunol. (1991) [Pubmed]
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