Myelin oligodendrocyte glycoprotein immunoglobulin G‐associated disease: An overview
2018
Myelin oligodendrocyte glycoprotein(MOG) is localized at the outermost layer of the
myelin sheathand is accessible for autoantibodies. Although experimental
autoimmune encephalitisinduced with MOG immunization has been studied for 30 years, the results of previous reports on MOG immunoglobulin G (IgG) detection with enzyme-linked immunosorbent assay and Western blot are confusing. However, after the development of human MOG-transfected cell-based assay to detect conformational-sensitive MOG-IgG, unique groups of patients have been found seropositive, and MOG-IgG-associated disease has become a hot topic in clinical
neuroimmunology. Currently, the clinical spectrum of MOG-IgG-associated disease includes idiopathic
optic neuritis,
acute disseminated encephalomyelitis, encephalitides (brainstem and cerebral cortical), idiopathic
myelitis, atypical multiple sclerosis,
aquaporin-4IgG-negative
neuromyelitis optica
spectrum disordersand others. MOG-IgG-associated disease occurs in both children and adults, and the female:male ratio is almost 1:1.
Pleocytosisin the cerebrospinal fluids during acute exacerbation is often seen, but oligoclonal IgG bands are usually negative.
T helper cell17, B cells and neutrophil-related cytokines appear to be upregulated intrathecally. The pathology of acute lesions is characterized by active inflammation demyelination with deposition of immunoglobulins and complements. Just like
aquaporin 4IgG-positive
neuromyelitis optica
spectrum disorders, some disease-modifying drugs for multiple sclerosis seem to be inefficacious in MOG-IgG-associated disease, and chronic immunosuppression is required to prevent relapse, especially in patients persistently positive for MOG-IgG. Our understanding of this newly recognized disease remains insufficient, and the progress of research is much expected.
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