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In a cross between two mouse strains, the susceptible B10.RIII (H-2 r ) and resistant RIIIS/J (H-2 r ) strains, a locus on mouse chromosome 5 ( Eae39 ) was previously shown to control experimental autoimmune encephalomyelitis (EAE). Recently, quantitative trait loci (QTL), linked to disease in different experimental arthritis models, were mapped to this region. The aim of the present study was to investigate whether genes within  Eae39 , in addition to EAE, control development of collagen-induced arthritis (CIA).    Methods  CIA, induced by immunisation with bovine type II collagen, was studied in  Eae39  congenic and sub-interval congenic mice. Antibody titres were investigated with ELISA. Gene-typing was performed by micro-satellite mapping and statistics was calculated by standard methods.    Results  Experiments of CIA in  Eae39  congenic- and sub-interval congenic mice, carrying RIIIS/J genes on the B10.RIII genetic background, revealed three loci within  Eae39  that control disease and anti-collagen antibody titres. Two of the loci promoted disease and the third locus was protected against CIA development. By further breeding of mice with small congenic fragments, we identified a 3.2 mega base pair (Mbp) interval that regulates disease.    Conclusions  Disease-promoting and disease-protecting genes within the  Eae39  locus on mouse chromosome 5 control susceptibility to CIA. A disease-protecting locus in the telomeric part of  Eae39  results in lower anti-collagen antibody responses. The study shows the importance of breeding sub-congenic mouse strains to reveal genetic effects on complex diseases.

Dissection of a locus on mouse chromosome 5 reveals arthritis promoting and inhibitory genes