Mechanisms of action of auranofin: effects on humoral immune response.
Auranofin (AF) and gold sodium thiomalate (GSTM) were evaluated in antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent antibody responses. AF decreased the ability of immune sera to participate in ADCC, whereas GSTM did not. Immune serum from AF-treated rats also exhibited a decreased antibody-dependent complement lysis (ADCL) reactivity. In contrast, immune sera from GSTM-treated rats enhanced ADCL. AF also suppressed '7S' hemagglutinin antibody response to sheep red blood cells in adjuvant arthritic rats, whereas neither GSTM nor gold sodium thioglucose significantly suppressed hemagglutinin antibody titers at doses which produced antiinflammatory activity.
D000818:Animals; D000906:Antibodies / Q000276:immunology; D000917:Antibody Formation / Q000187:drug effects*; D000920:Antibody-Dependent Cell Cytotoxicity / Q000187:drug effects; D001169:Arthritis, Experimental / Q000276:immunology; D001310:Auranofin; D006051:Aurothioglucose / Q000031:analogs & derivatives* / Q000494:pharmacology; D001696:Biomechanical Phenomena; D003165:Complement System Proteins / Q000276:immunology / Q000378:metabolism; D006046:Gold / Q000031:analogs & derivatives*; D006052:Gold Sodium Thiomalate / Q000494:pharmacology; D006384:Hemagglutination; D051381:Rats; D011919:Rats, Inbred Strains
D000906:Antibodies; D006052:Gold Sodium Thiomalate; D006051:Aurothioglucose; D001310:Auranofin; D006046:Gold; D003165:Complement System Proteins