Bromodeoxyuridine and light treatment deletes effector but not suppressor cells of autoimmune encephalomyelitis.

Spleen cells (SpC) from Lewis rats that have recovered from experimental autoimmune encephalomyelitis (EAE) confer protection against EAE to naive syngeneic recipients if transferred directly (without culture), but transfer EAE if first activated in culture in the presence of myelin basic protein (MBP) antigen. In order to test the hypothesis that both effector (Te) and suppressor (Ts) cells of EAE coexist in recovered rats, but only the Te proliferate in culture in response to MBP, bromodeoxyuridine (BUdR) was added to the culture and dividing cells were killed by exposure to light prior to adoptive transfer. Recipients of BUdR+light-treated cells did not develop EAE, showing that Te were deleted by the treatment. In contrast, Ts activity persisted because these recipients were protected against EAE when challenged with an encephalitogenic dose of MBP.