Effect of HgCl2 on experimental allergic encephalomyelitis in Lewis rats. HgC12i-nduced down-modulation of the disease

HgC12 induces autoimmunity in Brown-Norway rats and immunosuppression in Lewis rats. In the latter rats, HgC12 triggers the proliferation of T suppressor/cytotoxic (OX8+) cells which actively suppress T cell functions. This led us to study the effect of HgC12 on experimental allergic encephalomyelitis (EAE), a T cell-mediated autoimmune disease obtained following immunization with basic protein (BP). It will be shown that HgC12 attenuates or even prevents clinical manifestations of EAE and inhibits both the proliferative response of T cells to BP and the anti-BP antibody response. This immunosuppression was not due to a defect at the T helper cell or antigen-processing cell level but to the emergence of T suppressor cells.