The myelin sheath, a lipid‐rich multilamellar membrane of relative stability, both insulates and enhances conduction in nerve axons. A notable feature of myelin‐specific proteins, in particular myelin basic protein, is their susceptibility to prote‐olytic activity and their encephalitogenicity, which induces inflammatory demyelination in the CNS. The final common pathway of myelin breakdownin vivais well documented and there is evidence that myelin disruption can be mediated directly by soluble (circulating) factors and for following receptor‐driven phagocytosis by macrophages. However the exact mechanism(s) of demyelination in multiple sclerosis is still unresolved, both antigen‐specific and ‐ non‐specific events having the potential to generate the myelino
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