The Y-linked autoimmune accelerating gene mutation (yaa), first discovered in 
the BXSB mouse strain, is known to accelerate spontaneous autoantibody 
production and subsequent development of lupus disease. We have investigated the 
role of the yaa gene in the development of the type II collagen (CII)-induced 
arthritis (CIA), which is used as a model for rheumatoid arthritis. In contrast 
to the accelerating effects on development of lupus autoimmunity we can show 
that the presence of BXSB Y chromosome carrying the yaa gene block development 
of CIA in F1 crosses with three normally CIA-susceptible strains, DBA/1, C3H.Q 
and B10.Q. Backcross experiments showed an additional modulatory effect from 
other BXSB genes or possibly from DBA/1 X chromosome. To evaluate the effect 
mediated by the yaa gene alone, the BXSB Y chromosome was bred into the DBA/1 
gene background. The DBA/1 congenic DBA/1.yaa male mice were less susceptible to 
arthritis development than their DBA/1 counterparts. (B10.QxDBA/1.yaa)F1 
acquired resistance to arthritis development similar to that of DBA/1.yaa, 
indicating a role for the yaa gene alone. The serum levels of autoantibodies to 
CII were significantly suppressed in all strains carrying yaa. In DBA/1.yaa mice 
a reduced number of T cells were found to produce interferon-gamma after in 
vitro stimulation with CII. Thus, although autoreactive B cells are important in 
both diseases they play different roles in murine lupus and in CIA.