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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.

Journal of Immunology 146(4): 1375-1379

1991

ISSN/ISBN: 0022-1767
PMID: 1991974
Document Number: 379043
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.

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