Chronic-relapsing experimental autoimmune encephalomyelitis. Myelin basic protein induces suppression of blastogenesis during remissions but not during exacerbations.

Previous work from this laboratory has shown that resistance to acute experimental autoimmune encephalomyelitis (EAE) correlates with disease-specific, antigen-induced suppression of blastogenesis in vitro. We now report that this suppression in vitro also occurs during remissions in animals with chronic-relapsing EAE. Hartley strain guinea pigs were injected with an homogenate of guinea pig spinal cord in complete Freund's adjuvant (CFA) to induce EAE or, for control purposes, with CFA alone. Animals injected with spinal cord homogenate developed EAE. Susceptible animals displayed up to 3 exacerbations over 4-5 months. Spleen cells and nervous tissue were sampled from different animals during and after each exacerbation. Gross examination of nervous tissue revealed plaques that at the light microscope level were characteristic of chronic-relapsing EAE. Lymphocyte transformation assays using the T-cell mitogen concanavalin A (Con A), guinea pig myelin basic protein (BP), the purified protein derivative of M. tuberculosis (PPD) and histone proteins were conducted. Results of these assays showed that in spleen cells from animals sampled during remissions, BP suppressed the Con A response. Similar suppression was not observed with spleen cells from animals in exacerbation. This suppression depended upon the presence of adherent cells. Neither PPD nor histone proteins suppressed the Con A response. Thus, an immunologic mechanism, similar to that observed in Hartley guinea pigs resistant to acute EAE, is also found during remissions in the chronic-relapsing form of this disease suggesting that both resistance and remission are mediated by an antigen-induced suppressor mechanism.