SummaryPVG/c rats, infected 3 days previously with 103Trypanosoma brucei brucei S.42 organisms failed to develop adjuvant disease in response to an intradermal inoculation of mycobacterial adjuvant. By contrast, similarly infected rats, immunized with heterologous brain and spinal cord in Freund's complete adjuvant with pertussis vaccine as a secondary adjuvant, developed clinical signs of allergic encephalomyelitis (EAE) at least as severe as those in uninfected rats.Delayed hypersensitivity reactions to PPD were depressed in trypanosome‐infected, adjuvant‐injected rats, as were the reactions to myelin basic protein in infected rats developing EAE. There appeared to be no cross‐reactivity between trypanosomal antigen and myelin basic protein which could account for the lack of suppression of EAE.It is suggested that the different extent to which autoimmunity is involved in these two experimental allergic diseases may account for the differential suppressive activity of trypanosome infections upon