Abstract
Demyelinating diseases of the CNS are a result of an autoimmune attack to the myelin sheaths surrounding axons. Their structural proteins become antigenic and as a result, myelin lesions appear. The identification of specific antibodies directed against the components of myelin, using highly specialized methods of laboratory diagnostics, can significantly improve diagnostic approaches. Currently, myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) consists of demyelinating syndromes with an identified antigen. The pathogenic role of human MOG-IgG has been demonstrated, which makes it possible to isolate this disease into a separate nosological form. However, for the myelin oligodendrocyte glycoprotein (MOG) gene, alternative splicing can produce various isoforms, which hinders antigen detection even for the most advanced techniques of immunofluorescence analysis. On the other hand, MOG conformational changes provide the structural integrity of other myelin proteins and maintain immune autotolerance mechanisms that are unique to humans.
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