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 (chi(2) = 15.68, p = 7.5 x 10(-5)), as was D1Mit12 at 
63.1 cM (chi(2) = 20.17, p = 7.1 x 10(-6)). D1Mit403 at 100 cM was linked to 
anti-dsDNA Ab production (chi(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.