2 MODELS FOR MULTIPLE-SCLEROSIS - EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS AND THEILER MURINE ENCEPHALOMYELITIS VIRUS

In this review, we compare and contrast two popular models for multipl e sclerosis (MS), Theiler's murine encephalomyelitis virus (TMEV) dise ase and experimental allergic encephalomyelitis (EAE). These models ar e used to investigate the viral and autoimmune etiology of MS, respect ively. Infection with live TMEV is an essential component of TMEV demy elinating disease. TMEV-specific cellular and humoral immunity and apo ptosis of infected cells eliminate virus from the gray matter of the c entral nervous system (CNS) during the acute phase of TMEV disease. In contrast, during the chronic phase, TMEV persistently infects glial c ells and/or macrophages in the white matter. During the chronic phase, recruitment of macrophages, TMEV-specific T cells and antibody, with the induction of apoptosis are harmful to the host, leading to inflamm ation and demyelination. In EAE, induction of encephalitogenic CD4+ T cells is an important component for disease: After stimulation and act ivation, these T cells upregulate adhesion molecules and are able to e nter the CNS. Thl cytokines augment the recruitment of mononuclear cel ls in the CNS. Macrophages and/or glial cells secrete cytotoxic factor s leading to demyelination in conjunction with B cells secreting anti- myelin antibody. Although immunopathological pathways during the cours e of the demyelination in TMEV infection and EAE are not always the sa me, oligodendroglial apoptosis is observed in both models, suggesting that their demyelinating processes share a common terminal pathway and finally lead to quite a similar clinical and pathological picture.