The refractory phase of experimental allergic encephalomyelitis in the Lewis rat is antigen specific in its induction but not in its effect.

Rats that have recovered from experimental allergic encephalomyelitis (EAE) are refractory to attempts to induce further episodes of the disease. The specificity of this refractoriness was examined by determining the susceptibility of such animals to the related disease experimental allergic neuritis (EAN). As EAE and EAN are induced respectively by central nervous system myelin basic protein (MBP) and the P2 peptide of peripheral nerve myelin, it was possible to test whether the refractory phase of EAE represented a generalized hyporeactivity to antigenic challenge or was solely a failure to respond to the antigen with which disease was induced. For some experiments the roles of the two antigens were reversed, i.e. the effects of preimmunizing with P2 peptide on the susceptibility to EAE was examined. Animals preimmunized with MBP or P2 peptide became profoundly refractory to EAE and EAN respectively and rats preimmunized with one antigen but challenged with the other were susceptible to the challenge. It is concluded that refractoriness to EAE and EAN is largely antigen specific. Preimmunization with one antigen followed by challenge with a mixture of both suggested that the immunosuppression responsible for refractoriness, although specific in its induction, was non-specific in its effect.