Upon treatment with
HgCl2, H-2s mice, such as B10.S, develop an activation of B lymphocytes that depends, at least partially, on activation of T helper type 2 (Th2) cells and results in increased serum levels of
IgG1 and
IgE, appearance of
IgG autoantibodies, and development of immune
glomerulonephritis and
vasculitis. Results of previous studies and of experiments presented here indicate that the B cell activation and systemic
autoimmune disease fail to develop in MHC-congenic B10.D2 (H-2d) and B10.BR (H-2k) mice treated with
HgCl2, although B10.D2 T cells showed signs of activation by and specificity for
HgCl2 comparable to those seen in strain B10.S. Here, we report that following
HgCl2 injections the antibody response to sheep erythrocytes is normal in B10.S, but suppressed in B10.D2 mice. This suppression was prevented by MoAb to mouse IFN-gamma. Conversely, treatment of B10.D2 mice with murine recombinant IFN-gamma (rIFN-gamma) was able to reproduce the immunosuppression seen after
HgCl2 treatment. In B10.S mice, it took administration of both rIFN-gamma and
HgCl2 to suppress the anti-sheep erythrocyte response. Although rIFN-gamma diminished the increase in
IgE serum levels of HgCl2-treated B10.S mice, it failed to prevent their
autoantibody production and immune
glomerulonephritis. These findings further strengthen the concept that B10.S mice react to
HgCl2 by preferential activation of their Th2 cells producing
IL-4, whereas B10.D2 mice react to
HgCl2 by preferential activation of their Th1 cells, which produce IFN-gamma and thus suppress antibody responses.