To assess the capacity of major histocompatibility complex (MHC) class II‐binding competitor peptides in inhibiting antibody‐mediated disease processes, we studied experimental autoimmune myasthenia gravis in Lewis rats. Experimental autoimmune myasthenia gravis, a disease model mediated by T cell‐dependent autoantibodies against acetylcholine receptors, was induced by immunization with Torpedo californica acetylcholine receptor emulsified in complete Freund's adjuvant. The immunodominant acetylcholine receptor T cell epitope was recognized by T cells in the context of MHC class II RT1.B^L. The disease inhibitory capacity of RT1.B^L‐binding peptides not related to the acetylcholine receptor was determined upon co‐immunization with Torpedo acetylcholine receptor. Co‐immunization of peptide OVA323–339, a strong RT1.B^L‐binding competitor peptide, resulted in complete disease inhibition. Although, the priming of the anti‐acetylcholine receptor T cell response was not fully inhibited, the kinetics of the response was changed. Moreover, besides a drastic reduction of the anti‐Torpedo acetylcholine receptor antibody titers, a shift in isotype distribution was found. These findings indicate that antibody‐mediated autoimmune processes can be suppressed by MHC class II competitor peptides. Furthermore, the administration of such peptides in vivo not only passively inhibits T cell activation, but also functionally alters the immune response.