![]() ![]() Peschl, P., Bradl, M., Hoftberger, R., Berger, T. T- and B cell responses to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis and multiple sclerosis. Iglesias, A., Bauer, J., Litzenburger, T., Schubart, A. The magnitude and encephalogenic potential of autoimmune response to MOG is enhanced in MOG deficient mice. Myelin/oligodendrocyte glycoprotein-deficient (MOG-deficient) mice reveal lack of immune tolerance to MOG in wild-type mice. CNS myelin induces regulatory functions of DC-SIGN-expressing, antigen-presenting cells via cognate interaction with MOG. Identification of the myelin oligodendrocyte glycoprotein as a cellular receptor for rubella virus. The myelin oligodendrocyte glycoprotein directly binds nerve growth factor to modulate central axon circuitry. The structure and function of myelin oligodendrocyte glycoprotein. Signaling cascades activated upon antibody cross-linking of myelin oligodendrocyte glycoprotein: potential implications for multiple sclerosis. Splice variation in the cytoplasmic domains of myelin oligodendrocyte glycoprotein affects its cellular localisation and transport. Spatio-temporal transcriptome of the human brain. Complex alternative splicing of the myelin oligodendrocyte glycoprotein gene is unique to human and non-human primates. Myelin/oligodendrocyte glycoprotein is a member of a subset of the immunoglobulin superfamily encoded within the major histocompatibility complex. Differential ultrastructural localization of myelin basic protein, myelin/oligodendroglial glycoprotein, and 2ʹ,3ʹ-cyclic nucleotide 3ʹ-phosphodiesterase in the CNS of adult rats. The first demonstration of the pathogenicity of MOG-Abs.īrunner, C., Lassmann, H., Waehneldt, T. Augmentation of demyelination in rat acute allergic encephalomyelitis by circulating mouse monoclonal antibodies directed against a myelin/oligodendrocyte glycoprotein. ![]() Linington, C., Bradl, M., Lassmann, H., Brunner, C. Presence of anti-M2 antibodies in central nervous system tissue and the possible role of M2 autoantigen in the induction of the disease. Chronic experimental autoimmune encephalomyelitis in the guinea pig. Investigation of human MOG-Ab pathogenicity is hampered by their limited binding to rodent MOG nevertheless, the place of MOG-Ab-associated disorders in the spectrum of inflammatory demyelinating diseases is becoming clearer. Many patients develop relapsing disease relapses usually involve optic neuritis and often occur during steroid weaning or soon after steroid cessation, suggesting that a longer initial treatment duration is required. Most patients with MOG-Ab-associated disorders have favourable outcomes, but a subset are left with permanent disability, usually as a result of the initial attack. The clinical presentation of MOG-Ab-associated disorders changes with age: MOG-Abs are associated with an ADEM-like presentation in young children and an opticospinal presentation in children aged >9 years and adults. MOG-Ab-associated disorders account for a larger proportion of paediatric patients than that of adult patients who present with acquired demyelinating disease. We also highlight differences between MOG-Ab-associated disease, NMOSD and MS, and describe our current understanding on how best to treat MOG-Ab-associated disease.Īntibodies against myelin oligodendrocyte glycoprotein (MOG-Abs) that are detectable with cell-based assays are associated with non-MS acquired demyelinating syndromes of the CNS. We collate the data on antibody pathogenicity and the mechanisms that are thought to underlie this. This Review provides an overview of the current knowledge of MOG, the metrics of MOG-Ab assays and the clinical associations identified. MOG-Ab-associated disease is different to AQP4-Ab-positive NMOSD and MS. The clinical phenotypes, disease courses and responses to treatment that are associated with MOG-Abs are currently being defined. ![]() This shift in our understanding of the diagnostic assays has re-invigorated the examination of MOG-Abs and their role in autoimmune and demyelinating disorders of the CNS. Further studies identified MOG-Abs in adults and children with ADEM, seizures, encephalitis, anti-aquaporin-4-antibody (AQP4-Ab)-seronegative neuromyelitis optica spectrum disorder (NMOSD) and related syndromes (optic neuritis, myelitis and brainstem encephalitis), but rarely in MS. Initially, MOG-Abs were reported in children with acute disseminated encephalomyelitis (ADEM). Use of cell-based assays with native MOG as the substrate enabled identification of a group of MOG-Ab-positive patients with demyelinating phenotypes. Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies (MOG-Abs) were first detected by immunoblot and enzyme-linked immunosorbent assay nearly 30 years ago, but their association with multiple sclerosis (MS) was not specific. ![]()
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