Experimental SLE can be induced in susceptible mice by their immunizat
ion with the human monoclonal anti-DNA antibody that bears a major idi
otype-16/6 Id. The SLE afflicted mice produce a variety of autoantibod
ies including anti-DNA antibodies. It was of interest to find out the
effect of DNA on the induction of the experimental disease. To this en
d, mice were immunized with combinations of 16/6 Id and DNA. The resul
ts indicated that whereas mice primed with 16/6 Id developed high tite
rs of antibodies to the 16/6 Id and a variety of autoantibodies typica
l to the experimental SLE, preimmunization of mice with ssDNA led to a
reduction in the 16/6 Id specific antibodies and in the autoantibody
titers. No significant differences could be detected in the clinical m
anifestations which are present in the mice with experimental disease
(increased erythrocyte sedimentation rate, leukopenia, proteinuria and
glomerular immune complex deposition) in all mice immunized with 16/6
Id including those pretreated with DNA. Thus, no direct correlation e
xists between the autoantibody levels and the clinical pathology, and
probably other factors are involved in the development of the experime
ntal disease.