Lewis rats, treated from birth with a rabbit anti-rat IgM antiserum are B-cell and immunoglobulin deficient. When sensitized with myelin basic protein (BP) and complete Freund's adjuvant (CFA), these rats do not make detectable antibodies to BP, nor do they develop clinical or histopathological evidence of allergic encephalomyelitis (EAE). We show here that transfer of anti-BP antibody containing serum to BP sensitized Ig deficient rats results in subsequent development of EAE. We also demonstrate that BP sensitized Ig deficient rats which do not develop EAE, nevertheless generate effector cells capable of transferring disease, and thus specific T-cell function is not inhibited by the anti-Ig treatment. Finally, Ig deficient rats were shown to be perfectly adequate recipients of passively induced EAE.