Experimental autoimmune myasthenia gravis (EAMG) is a well established animal model, which can be induced in various animal species and strains with acetylcholine receptor (AChR) and represents an experimental counterpart of human myasthenia gravis (MG). Current im-munotherapies to both EAMG and MG are non specific and limited by their toxicity. Recently, toler-ance to EAMG has been achieved by oral administration of milligram quantities of Torpedo AChR. In the present report we demonstrate that nasal administration of microgram doses of Torpedo AChR to female Lewis rats prior to immunization with Torpedo AChR and complete Freund’s adjuvant resulted in the prevention of subsequently induced EAMG, the suppression of serum anti - AChR antibody levels, the decrease of delayed -type hyersensitjvity responses to AChR, as well as the suppression of AChR -specific IgG secreting cells, AChR -reactive IFN -r secreting cells and T cell proliferation in peripheral lymphoid organs, particularly in popliteal and ing Experimental autoimmune myasthenia gravis (EAMG) is a well established animal model, which can be induced in various animal species and strains with acetylcholine receptor (AChR) and represents an experimental counterpart of human myasthenia gravis (MG). Current im-munotherapies to both EAMG and, are non specific and limited by their toxicity. Recently, toler-ance to EAMG has been achieved by oral administration of milligram quantities of Torpedo AChR. In the present report we demonstrate that nasal administration of microgram doses of Torpedo AChR to female Lewis rats prior to immunization with Torpedo AChR and complete Freund’s adjuvant resulted in the prevention of subsequent induced EAMG, the suppression of serum anti-AChR antibody levels, the decrease of delayed-type hyersensitvity response to AChR, as well as the suppression of AChR-specific IgG secreting cells, AChR-reactive IFN-r secreting cells and T cell proliferation in peripheral lymphoid organs, particularly in popliteal and ing