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Multiple sclerosis (MS)

Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are inflammatory diseases of the central nervous system (CNS) characterized by localized areas of demyelination. MS is believed to be an autoimmune disorder mediated by activated immune cells such as T- and B-lymphocytes and macrophages/microglia. Lymphocytes are primed in the peripheral tissues by antigens, and clonally expanded cells infiltrate the CNS. They produce large amounts of inflammatory and cytokines that lead to demyelination and axonal degeneration [1].

MS is a chronic, demyelinating disease of the CNS in which autoimmunity to myelin plays a role in pathogenesis. The epidemiology of MS indicates that it may be triggered by a virus infection before the age of adolescence, but attempts to associate a specific virus with MS have produced equivocal results [2].

Semliki Forest virus (SFV) infection induces a demyelinating encephalomyelitis in the CNS of mice and serves as a model for MS. CD8(+) T cells are involved in the initial destruction of CNS tissue during the first weeks of SFV infection, while B cells, antibodies and microglia may contribute to the myelin pathology seen after recovery [3].

IMGT reference:
[1] Hisahara, S, et al., Neurosci Res., 46, 387-397 (2003) PMID:12871760
[2] Atkins, GJ, et al., Rev Med Virol., 10, 291-303 (2000) PMID:11015741
[3] Mokhtarian, F et al., J Neuroimmunol., 137, 19-31 (2003) PMID:12667644