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*
Rheumatology Section and Departments of
Histopathology and
Transplantation Biology, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom
BXSB mice spontaneously develop a lupus-like syndrome that is
accelerated by the Yaa gene (Y-linked autoimmune
accelerator). We studied the phenotype of disease in (B10 x
BXSB)F1 and (BXSB x (B10 x BXSB)F1)
backcross mice and genotyped 224 backcross animals to allow a
microsatellite-based genome-wide linkage analysis to be conducted. In
the backcross population, three intervals on chromosome 1 showed
significant linkage to disease, suggesting that multiple loci
contribute to the production of autoimmune disease.
D1Mit5 at 32.8 cM was linked to development of nephritis
(
2 = 15.68, p = 7.5 x
10-5), as was D1Mit12 at 63.1 cM
(2 = 20.17, p = 7.1 x
10-6). D1Mit403 at 100 cM was linked to
anti-dsDNA Ab production (2 = 17.28,
p = 3.2 x 10-5). Suggestive
linkages to antinuclear Abs and nephritis were identified on chromosome
3, to splenomegaly on chromosome 4, and to anti-ssDNA Ab production
on chromosome 10. Chromosome 4 and the telomeric region of chromosome 1
have previously been linked to disease in other mouse models of
systemic lupus erythematosus; however, the centromeric regions of
chromosome 1 and chromosomes 3 and 10 are unique to BXSB. This implies
that, though some loci may be common to a number of mouse models of
lupus, different clusters of disease genes confer disease
susceptibility in different strains of mice.
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