Experiments examining the role of IL-2 receptor bearing cells in experimental allergic encephalomyelitis (EAE) were performed using the chimeric protein IL2-PE40 which is cytotoxic for the above mentioned cells. Early treatment of mice with IL2-PE40 (1-4 days post-transfer of encephalitogenic lymphocytes) prevented the expression of clinical signs of EAE. Administration of IL2-PE40 at the onset of clinical symptoms significantly reduced the severity of disease and also prevented the subsequent development of relapses. This treatment also resulted in decreases in the level of demyelination and in the degree of inflammatory responses observed in the brain and spinal cord. Immunization of SJL mice donors with myelin basic protein (MBP) resulted in the generation of MBP-specific T lymphocyte responses. After in vitro culture with MBP, these cells passively transferred EAE into naive recipients. UV irradiation of donor mice resulted in strong suggression (70-80%) of the immune response, as measured by MBP-specific proliferative responses of immune T cells. It was also observed that UV irradiation of recipient mice (prior to passive transfer of MBP-specific T cells) suppressed both the incidence and severity of disease.
