Previously we have shown that antibodies and T cells against myelin basic protein (MBP) from animals with EAE also recognize the specific synaptosomal protein synapsin I. These antibodies and T cells correlate with the appearance of the clinical symptoms of the disease. Intraperitoneal administration of low doses of soluble synaptosomal proteins, 10 and 3 days prior to the active induction of the disease, diminished the incidence and severity of EAE, reverted the appearance of CNS histological and biochemical alterations and changed the pattern of humoral response against MBP. In order to elucidate the mechanism underlying this suppressor effect, we also examined the proliferative and IL-2, IL-4, IL-10 secretion response to MBP of lymph node mononuclear cells (MNC) derived from treated animals and their ability to modulate the disease by passive transfer experiments. Cells from sick non-treated EAE rats show cell proliferation to MBP and a mixed pattern of cytokine secretion. Specific T cells to MBP are also present in treated rats but no IL-2 release was observed. Finally, lymph node MNC from treated animals were able to reduced the severity and delayed the onset of the disease when they were adoptively transferred to naive animals, prior to the induction of the disease. Therefore, the modulation of EAE induced by synaptosomal antigens involves an active suppression mechanism mediated by regulatory cells and constitutes an evidence about the putative participation of these extra-myelin antigens in the pathogenesis of EAE.
