Experimental allergic encephalomyelitis (EAE) can be transferred by spleen cells stimulated in vitro with D-mannose-binding lectins but not with N-acetyl-D-galactosamine (GalNAc)-binding lectins. EAE could also be passively transferred by spleen cells following incubation with wheat germ agglutinin (WGA), in which case the disease transfer was abolished by the specific hapten inhibitor, N-acetyl-D-glucosamine. In the presence of rat T cell monoclonal antibody, either W3/25 or OX-8, both concanavalin A and Wisteria floribunda agglutinin stimulated helper and suppressor T subpopulations. On the other hand, GalNAc-binding lectins were less effective than D-mannose-binding lectins in generating interleukin 2 (IL2) in the culture supernatant, whereas WGA-stimulated spleen cells did not produce IL2. Furthermore, spleen cells cultured with pure IL2 could not transfer EAE to the recipients. These data suggest that some factors distinct from IL2 are required for the differentiation of EAE-effector precursors into the final effector cells in this transfer system.