To understand the role of TNF-α in the induction of experimental autoimmune myasthenia gravis (EAMG) and detect a possible effect of anti-TNF-α antibodies in the treatment of EAMG, anti-TNF-α antibodies were administrated intraperitoneally to Lewis rats twice per week for 5 weeks from the day of immunization with Torpedo AChR and complete Freund's adjuvant (CFA). Administration of anti-TNF-α antibodies resulted in lower incidence of EAMG, and in delayed onset and only mild muscle weakness compared with control EAMG rats. These mild clinical signs were accompanied by lower AChR-specific lymphocyte proliferation, down-regulated IFN-γ and IL-10, and up-regulated TGF-β. The lower levels of anti-AChR IgG, Ig2a and IgG2b and decreased anti-AChR IgG affinity were found in rats treated with anti-TNF-α antibodies. These results demonstrate that anti-TNF-α antibodies can suppress the induction and development of EAMG.