T-CELL NECESSITY IN PATHOGENESIS OF EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS IN MICE

Cellular transfer of experimental autoimmune encephalomyelitis (EAE) was effected in mice with lymph node and spleen cells from appropriately immunized donors. Immune serum did not transfer this autoimmune disease, nor did serum have any facilitating or inhibitory effect on the capacity of lymphoid cells to transfer EAE. Transfer of EAE was effected in normal mice, lightly irradiated (350 rad) and lethally irradiated (850 rad) and bone marrow-protected mice, but not in mice given 850 rad to total-body irradiation. There was a striking augmentation of severity of transferred EAE in the lightly irradiated recipients, possibly attributable to selective radiosensitivity of suppressor T [thymus-derived] cells. Cell-mediated immunity but not circulating antibody to basic protein of myelin was demonstrated in recipients with transferred EAE. The immune lymphoid cells responsible for transfer of EAE were T lymphocytes. Thus, transfer was successful after passage of sensitized cells through anti-immunoglobulin columns, and was abrogated following treatment with anti-Thy-1 serum and complement. Neonatally thymectomized mice failed to develop EAE, cell-mediated immunity or humoral antibody against myelin basic protein (BPM). Inhibition of EAE and immune responsiveness was solely due to the removal of the source of thymus lymphocytes, because reconstitution of neonatally thymectomized mice with T lymphocytes completely restored these functions. T lymphocytes are required for the production and adoptive transfer of EAE, for the development of cell-mediated immunity to BPM, and for the production of antibody to BPM.