Anti-myelin antibodies, IgG

Anti-myelin antibodies, IgG (myelin-specific autoantibodies) testing is used as an adjunct in the diagnostic workup of multiple sclerosis and other central nervous system demyelinating disorders. The assay also supports prognostic assessment and tracking of treatment response and disease activity. Results require correlation with examination findings, MRI, and additional laboratories because these antibodies are not specific for multiple sclerosis and can occur in other demyelinating conditions and after stroke.

Immune-mediated damage to the myelin sheath underlies central nervous system demyelinating disorders. Although T-cell mechanisms dominate, humoral immunity directed at myelin antigens contributes to pathogenesis in a subset of patients. The spectrum of anti-myelin antibodies includes several defined targets. Anti–myelin oligodendrocyte glycoprotein (MOG) recognizes a surface glycoprotein accessible to antibodies and capable of binding C1q. Anti–myelin basic protein (MBP) binds a major intracellular myelin protein; its direct pathogenic role remains uncertain. Anti–myelin-associated glycoprotein (MAG) is classically linked to demyelinating neuropathies with monoclonal gammopathy but has also been reported in multiple sclerosis (MS). Antibodies to galactocerebroside, a principal myelin lipid, have been associated with demyelination and are more typical of relapsing–remitting MS. Anti–proteolipid protein (PLP) targets another abundant myelin component. In addition, cerebrospinal fluid oligoclonal IgM against phosphatidylcholine has been associated with a more aggressive clinical course. Anti-MOG antibodies are detectable in serum and CSF of patients with MS and are reported more often in pediatric-onset MS; several studies suggest that titers may reflect disease activity. In selected cohorts, anti-MBP may complement anti-MOG in estimating the likelihood that clinically isolated syndrome will convert to MS. Anti-myelin antibodies are not specific for MS; they may be seen in other demyelinating syndromes (for example, Marburg disease and acute disseminated encephalomyelitis) and can persist after stroke. Accordingly, they function as adjunctive markers and should be interpreted alongside comprehensive clinical and imaging data.