Continuous blockade of B-cell antigen receptors (BCRs) with Fab alpha
sIg prevents the anti-ssDNA response of high, but not low, density B c
ells. Signaling via the BCRs, by prior exposure to crosslinking F(ab')
2 alpha sIg, had no effect on the spontaneous anti-DNA response, but p
revented a lipopolysaccharide-induced anti-DNA response. Pretreatment
with intact alpha sIg, which provides exogenously derived Fc signals,
reduced the response. An Fc-signal-blocking agent, F(ab')2 anti-IgG-Fc
antibody, increased the number of anti-DNA antibody-forming cells pro
duced in the absence of exogenous IgG anti-ssDNA antibody. Thus, activ
ation is dependent on the availability of the BCRs, prior BCR crosslin
king does not interfere with activation, and endogenous IgG anti-ssDNA
antibody limits the activation of anti-ssDNA-specific B cells most of
which are T-cell independent. These results indicate that the anti-ss
DNA response is driven through the BCR.