[The pathogenic mechanism of experimental autoimmune encephalomyelitis and approach for new immunological therapy]

Experimental autoimmune encephalomyelitis (EAE) is an autoimmune disease mediated by myelin protein-specific CD4 T cells of the Th 1 phenotype and is a major animal model for the study of multiple sclerosis. Here we review current research advancements on the pathogenic mechanism of disease induction, remission and exacervasion. Progresses both in the molecular biology and immunology permit us to make a new strategy of specific therapy for EAE. There are three important strategies to prevent disease; the first is to block the trimolecular complex and associated accessory molecules to stop the T cell activation, the second is to regulate the activated T cells with immunological networking system and the third is to modulate the immunological responses mediated by T cells in the central nervous system.