In the present study, we mapped the major quantitative trait loci (QTL) 
differing between the NZW and C57BL/6 inbred strains of mice by making use of 
(NZW x C57BL/6.Yaa)F1 mice, a model in which the lupus-like autoimmune syndrome 
observed in male mice is associated with the presence of an as yet unidentified 
Y chromosome-linked autoimmune acceleration gene, Yaa. Linkage analysis of 126 
C57BL/6 x (NZW x C57BL/6.Yaa)F1 backcross males provided evidence for a major 
QTL on chromosome 7 controlling both the severity of glomerulonephritis and the 
production of IgG anti-DNA autoantibody and retroviral gp70-anti-gp70 immune 
complexes. Two additional QTL of C57BL/6 origin on chromosome 17 had no apparent 
individual effects, but showed strong epistatic interaction with chromosome 7 
QTL for disease severity and anti-DNA autoantibody production. Our data also 
identified on chromosome 13 a QTL of NZW origin with a major effect on the level 
of gp70, and showing an additive effect with the chromosome 7 QTL on the level 
of gp70 immune complexes. Our study thus provides a model to dissect the complex 
genetic interactions that result in manifestations of murine lupus-like disease.