Abstract
Experimental allergic encephalomyelitis (EAE) in the Lewis rat is an acute, self-limiting disease. Rechallenge of convalescent rats shortly after recovery leads to the reinduction of a mild, brief clinical episode. With increasing time after primary sensitization, rats become resistant to reinduction of both clinical and histologic signs of EAE. Convalescent rats that are resistant to reinduction of disease retain specific antigen-reactive cells, as evidenced by the ability of their lymphocytes to response in vitro to basic protein (BP). Spleen cells from convalescent rats can be used to reconstitute the lymphomyeloid apparatus of lethally irradiated rats. These reconstituted rats develop EAE in a normal fashion. These experiments provide evidence against clonal deletion as the mechanism of recovery from and resistance to reinduction of EAE and suggest the operation of an active suppressor mechanism. Although resistant to active reinduction of disease, convalescent rats do not appear to represent a suppressive environment for passive induction of disease. Sensitized lymphocytes capable of inducting EAE in naive recipients are not inactivated when transferred into convalescent recipients. The passively induced disease in convalescent rats is equal in severity to disease in naive recipients but shows a difference in the distribution of lesions with involvement of the cerebellum in the former but not the latter.