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individual is exposed, particularly in the far higher northern and southern latitudes This phenomenon of molecular mimicry (a shared antigen between the virus and CNS myelin, the oligodendrocyte, or cerebral vessels) has been invoked as a mechanism in several diseases, notably in rheumatic fever, certain paraneoplastic diseases, and Guillain-Barre syndrome, but remains speculative in MS The role of humoral and cellular factors in the production of MS plaques is not fully understood The deposition of immunoglobulin in the plaques of patients with acute and relapsing-remitting disease, but not those with progressive MS, has been alluded to earlier That the humoral immune system is involved is evident from the presence in the CSF of most patients of oligoclonal immune protein antibodies, which are produced by B lymphocytes within the CNS Sera from patients with MS (and some normal controls), when added to cultures of nervous system tissue from newborn mice in the presence of complement, can damage myelin, inhibit remyelination, and block axonal conduction Antibodies to oligodendrocytes are present in the serum of up to 90 percent of patients in some studies but far less frequently in others Of note also are the ndings of Berger and colleagues that show a relationship between the clinical progression of early and monosymptomatic MS and the presence of serum autoantibodies against oligodendrocyte glycoprotein and myelin basic protein They have reported that the absence of antibodies, a nding in 38 percent of their patients, identi ed a group with more benign disease, at least for several years Whether this further indicates, as they suggest, that humoral immune mechanisms are essential to the production of MS is uncertain Autoantibodies have been found that are directed against myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) It has also been demonstrated that subsets of T cells (CD41 Th2 cells) are activated by MBP and MOG to activate B cells, the production of oligoclonal bands and membrane attack complexes, and the release of cytokines [tumor necrosis factor alpha (TNF- ), interleukins, interferon gamma (IFN- )] The in ammatory process erodes the blood-brain barrier and ultimately destroys both oligodendroglia and axons The eventual functional outcome re ects both the activity of this in ammatory cascade and the degree of axonal damage In other cases, there may be a compromise of oligodendroglial function and axonal degeneration in the absence of prominent in ammation (see reviews by French-Constant and Hemmer) Nevertheless, most immunologists currently subscribe to the notion that MS is mediated by a T-cell sensitization to myelin This idea is supported by numerous lines of evidence including the observation that T cells initiate the lesions of experimental allergic encephalomyelitis (EAE), which is assumed to be an animal model of MS, as suggested by Adams Although the entry of autoreactive T cells into the CNS results in a perivascular in ammatory reaction, its relationship to MS is unclear Conceivably, intense T-cell stimulation is in itself suf cient to induce demyelination, but it is also possible that the primary target of the immune reaction is the myelin sheath or some component thereof and that the T-cell in ltration is the result of the demyelination Other investigators believe that an additional insult is required, as illustrated by the EAE animal model, in which myelin alone is not a suf cient factor but always requires an adjuvant immune stimulus EAE is clearly an imperfect model; it is not a naturally occurring disease but one in which a demyelination of the CNS is induced in susceptible animals in a single episode by autologous myelin antigens The.

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