
The antibody against myelin oligodendrocyte glycoprotein (MOG) has been identified for its association with several clinical phenotypes including acute or multiphasic disseminated encephalomyelitis, optic neuritis, NMOSD, and brainstem or cerebral cortical encephalomyelitis, and now generally called MOG associated disorders (MOGAD). Recent brain-biopsied MOG-antibody-positive case reports have suggested the dominance of humoral immunity, and the humoral and cellular immune responses against MOG is elucidated to develop perivenous inflammatory demyelination. In this review, we will focus on the clinical, pathological, and treatment strategies for MOG-antibody-related diseases.
Optic Neuritis, Humans, Brain, Myelin-Oligodendrocyte Glycoprotein, Encephalomyelitis, Autoantibodies
Optic Neuritis, Humans, Brain, Myelin-Oligodendrocyte Glycoprotein, Encephalomyelitis, Autoantibodies
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