Abstract
BACKGROUND: Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an acquired inflammatory demyelinating disease with optic neuritis (ON) as the most frequent clinical symptom. The hallmark of the disease is the presence of autoantibodies against MOG (MOG-IgG) in the serum of patients. Whereas the role of MOG in the experimental autoimmune encephalomyelitis animal model is well-established, the pathogenesis of the human disease and the role of human MOG-IgG is still not fully clear. EVIDENCE ACQUISITION: PubMed was searched for the terms "MOGAD," "optic neuritis," "MOG antibodies," and "experimental autoimmune encephalomyelitis" alone or in combination, to find articles of interest for this review. Only articles written in English language were included and reference lists were searched for further relevant papers. RESULTS: B and T cells play a role in the pathogenesis of human MOGAD. The distribution of lesions and their development toward the optic pathway is influenced by the genetic background in animal models. Moreover, MOGAD-associated ON is frequently bilateral and often relapsing with generally favorable visual outcome. Activated T-cell subsets create an inflammatory environment and B cells are necessary to produce autoantibodies directed against the MOG protein. Here, pathologic mechanisms of MOG-IgG are discussed, and histopathologic findings are presented. CONCLUSIONS: MOGAD patients often present with ON and harbor antibodies against MOG. Furthermore, pathogenesis is most likely a synergy between encephalitogenic T and antibody producing B cells. However, to which extent MOG-IgG are pathogenic and the exact pathologic mechanism is still not well understood.