Auranofin-induced suppression of autoimmune antibody production and inflammation in genetically autoimmune-prone mice.

The gold compound auranofin and lobenzarit (CCA) were compared in regard to effects on development of an autoimmune-like disease in MRL/1 mice, which normally develop elevated levels of serum anti-DNA antibodies and rheumatoid factor as well as joint lesions similar to those seen in patients with rheumatoid arthritis. MRL/1 mice, which are genetically prone to development of autoimmune disease, were given auranofin or lobenzarit by gavage for 15 weeks, starting at 6 weeks of age. Mice were examined periodically for immunological abnormalities as well as histologic changes in articular joints. The auranofin-treated mice showed marked diminution in development of anti-DNA antibodies and serum rheumatoid factor as compared to control animals. Although higher than in the auranofin-treated animals, CCA-treated mice also had lower levels of serum autoantibodies than those seen in the control animals. Examination of limb joints for histopathologic changes indicated that the auranofin-treated animals developed only the slightest evidence of lesions as compared to control animals. CCA-treated mice also had a lessening of lesion development compared to control animals, but lesions were more developed than in auranofin-treated mice. This study indicates that auranofin is more effective than CCA in diminishing development of autoimmunity in MRL/1 mice.