| Abstract: | This study was conducted to determine whether a monoclonal antibody (MAb) specific for rat interleukin 2 receptors (IL 2R) inhibits the activation of effector T cells that adoptively transfer experimental allergic encephalomyelitis (EAE). MAb OX 39 appears to be specific for IL 2R because it binds to concanavalin A-activated, but not resting, rat lymphocytes and inhibits mitogen- and IL 2-induced proliferation of rat spleen cells. Moreover, this MAb inhibits the in vitro activation of effector cells of EAE by myelin basic protein when added to immune donor spleen cell at the start of 72-hr culture or after 24 hr, but not when added after 48 hr of culture. Other studies employed MAb W3/25, which reacts with the rat helper T cell subset and appears to define the rat homolog of the human CD4 marker present on T4-positive cells. MAb W3/25 also blocks in vitro activation of EAE effector cells, and this blocking effect can be abrogated by adding rat T cell growth factor or partially purified IL 2 to the donor spleen cell cultures. T cell growth factor alone is incapable of activating EAE effector cells. These findings are discussed with respect to the role of lymphokines in the generation of autoreactive T cells. |
