Failure of serum from recovered rats to prevent enhanced adoptive transfer of experimental allergic encephalomyelitis.
The rat is unique among species used for research on experimental allergic encephalomyelitis (EAE) because of the spontaneous recovery which occurs routinely after severe, almost fatal disease. The mechanism of recovery has never been adequately explained although it has been suggested that suppressor cells might play a role in this phenomenon. In another immune system (contact sensitivity) anti-idiotypic antibodies obtained during the recovery phase have been shown to have a protective effect. Adoptive transfer of EAE, which can be markedly enhanced by incubation of sensitized cells with antigen in vitro, offers a convenient tool for investigating mechanisms of recovery. With this system, we have attempted to suppress transfer of disease with serum obtained from recovered rats. In spite of various manipulations of the experimental protocol, including the use of serum plus complement before and after incubation of cells with antigen, we have been unable to demonstrate suppression of disease. We and others recently reported that cells from recovered rats are also capable of enhanced transfer. This permitted the use of autologous serum from individual cell donors. Even in this strictly autologous system, however, no inhibitory effect of serum could be detected.
D000818:Animals; D001323:Autoantibodies / Q000276:immunology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D006168:Guinea Pigs; D007116:Immunization, Passive; D007130:Immunoglobulin Idiotypes / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D051381:Rats; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D001323:Autoantibodies; D007130:Immunoglobulin Idiotypes