Immunologic Factors in the Suppression of Experimental Allergic Encephalomyelitis: Relevence to Multiple Sclerosis

Abstract

Numerous autoimmune diseases of both humans and animals have heen described over the past few decades, but probably none have received as much attention as experimental allergic encephalomyelitis (EAE). Progress has been achieved in the study of EAE with the discovery and isolation of the myelin basic protein (BP) antigen (l, 2, 3), determination of its complete amino acid sequence (4), the isolation and synthesis of disease-inducing peptides (5, 6) and clarification of immunopathologic events in EAE (T). Recently new developments have been made in firmly establishing EAE as a cell-mediated autoimmune disease which under appropriate conditions compares closely with multiple sclerosis in humans (8). Horizons have also been extended in our understanding of antigenic and disease-inducing sites of the molecule, and the role of immune cell populations in the induction and suppressing of EAE. The immunogenic sites of the BP molecule responsible for the induction of EAE in several animal species including the monkey, guinea pig, rat and rabbit have recently been reviewed (9). It is now established that EAE is mediated by effector T lymphocytes sensitized to small crucial regions of the BP polypeptide chain.