![]() ![]() Significantly, MOG-Ab alone did not induce inflammation or tissue destruction rather, their interdependence with T cells was required to develop their pathogenic potential. The ac cumulation of MOG-Ab has been described in CNS antigen-presenting cells with subsequent activation of autoreactive T cells, followed by the induction of peripheral autoreactive T cells. In addition, MOG-Ab belongs to the complement binding IgG1 subtype and has been found to activate the complement cascade, leading to complement-dependent destruction of MOG-expressing cells. Initial studies revealed a pathogenic effect of the humoral immune response against MOG (human MOG-Ab) these antibodies were able to induce the death of MOG-expressing cells as well as natural killer cell-mediated cell death, with the extent of cell damage dependent on antibody levels. Furthermore, purified IgG from MOG-IgG–positive patients, when incubated with oligodendrocytes in vitro, led to obvious cytoskeletal disorganization, further suggesting functional pathogenicity. In humans, high-titer MOG-immunoglobulin G (MOG-IgG) levels in serum samples seem to efficiently activate the complement cascade in vitro. Key words: Myelin oligodendrocyte glycoprotein, Demyelinating diseases, Neuromyelitis optica, Optic neuritis, Acute disseminated encephalomyelitis This review summarizes the data regarding MOG-Ab as an impending biological marker for discriminating between these diverse demyelinating CNS diseases and discusses recent developments, clinical applications, and findings regarding the immunopathogenesis of MOG-Ab-associated disorders. A humoral immune reaction against MOG was recently found in monophasic diseases and recurrent/multiphasic clinical progression, particularly in pediatric patients. Using specific cell-based assays, MOG-Ab is becoming a potential biomarker of inflammatory demyelinating disorders of the CNS. MOG-Ab is associated with a wider clinical phenotype not limited to neuromyelitis optica spectrum disorder, with most patients presenting with optic neuritis, acute disseminated encephalomyelitis (ADEM) or ADEM-like encephalitis with brain demyelinating lesions, and/or myelitis. Antibodies against myelin oligodendrocyte glycoprotein (MOG-Ab) have been found in some cases of these demyelinating diseases, particularly in children. All rights reserved.Inflammatory or immune-mediated demyelinating central nervous system (CNS) syndromes include a broad spectrum of clinical phenotype and different overlapping diseases. Herpes simplex virus Meningitis Myelin-oligodendrocyte glycoprotein antibody Optic neuritis Urinary retention.Ĭopyright © 2017 Elsevier B.V. Clinicians should thus consider testing for MOG antibodies in patients with post-infectious neurological symptoms due to an HSV infection. Our case supports a relationship between anti-MOG antibodies and ON triggered by an HSV infection. Finally, he was diagnosed with MOG antibody-positive bilateral ON and meningoganglionitis following an HSV infection. Serum anti-AQP4 antibodies were negative, but anti-MOG antibodies were positive. Following treatment with acyclovir and steroid pulse, he fully recovered. ![]() A spinal MRI showed leptomeningeal enhancement from the thoracic to lumbar vertebrae and abnormal enhancement of the 元 to S3 dorsal root ganglia without a change in intramedullary signals. Ophthalmological evaluation and brain magnetic resonance imaging (MRI) revealed bilateral ON. This is the first report of bilateral ON following a herpes simplex virus (HSV) infection associated with a positive MOG antibody.Ī 41-year-old man who initially presented with genital herpes developed allodynia in the Th2-Th5 and Th8-L2 areas, urinary retention, and painful visual loss in the left eye. Similar to NMO/NMOSD associated with AQP4 antibodies, preceding infections have been reported in patients with MOG antibody-positive ON. Myelin oligodendrocyte glycoprotein (MOG) antibody-positive optic neuritis (ON) and myelitis are recognized as important differential diagnosis of aquaporin-4 (AQP4) antibody-positive neuromyelitis optica (NMO)/NMO spectrum disorder (NMOSD). ![]()
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