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

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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]

References

  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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