Both CD4(+) and CD8(+) T cells are likely to contribute to the immunopathogenesis of cAD through the production of interleukin-13, interleukin-22 and interferon-γ. In both subsets, functional analysis of FoxP3(+) cells is essential to determine their role.

SUMMARYUpon treatment with HgCl 2 , H-2 s 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-2 d ) and B10.BR (H-2 k ) mice treated with HgCl 2 , although B10.D2 T cells showed signs of activation by and specificity for HgCl 2 comparable to those seen in strain B10.S. Here, we report that following HgCl 2 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-g. Conversely, treatment of B10.D2 mice with murine recombinant IFN-g (rIFN-g) was able to reproduce the immunosuppression seen after HgCl 2 treatment. In B10.S mice, it took administration of both rIFN-g and HgCl 2 to suppress the antisheep erythrocyte response. Although rIFN-g diminished the increase in IgE serum levels of HgCl 2 -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 HgCl 2 by preferential activation of their Th2 cells producing IL-4, whereas B10.D2 mice react to HgCl 2 by preferential activation of their Th1 cells, which produce IFN-g and thus suppress antibody responses.