
Glycoproteins as targets of autoantibodies in CNS inflammation: MOG and more. One of the most extensively studied is myelin oligodendrocyte glycoprotein (MOG), largely used in animal models to induce experimental demyelination 4 4. Several other CNS antigens have been evaluated as potential targets in autoimmune inflammatory CNS disorders. , the interest has grown in the development of new laboratory biomarkers that could be used in the differential diagnosis of CNS demyelinating conditions. A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis. Lennon VA, Wingerchuk DM, Kryzer TJ, Pittock SJ, Lucchinetti CF, Fujihara K et al. Since the identification of the anti-aquaporin-4 antibody (AQP4-IgG) and its strong association with neuromyelitis optica spectrum disorders (NMOSD) 3 3. Multiple sclerosis is only diagnosed after the exclusion of other etiologies given that it still lacks a reliable biomarker. The most frequent and extensively studied is multiple sclerosis (MS) and its diagnosis is based on clinical and magnectic resonance imaging (MRI) characteristics. Axonal damage in acute multiple sclerosis lesions. Ferguson B, Matyszak MK, Esiri MM, Perry VH. , axonal lesion and neurodegeneration 2 2. The idiopathic acquired inflammatory central nervous system (CNS) disorders are a heterogenous group of autoimmune conditions caused by inflammation, myelin loss 1 1. Neurite óptica esclerose múltipla glicoproteína mielina-oligodendrócito autoanticorpos doenças desmielinizantes Conclusão: Nossos achados sugerem que o MOG-IgG é um biomarcador de doença desmielinizante diferente da EM. A ressonância magnética de encéfalo de todos os pacientes MOG-IgG positivos foi normal ou demonstrou apenas lesões inespecíficas em T2. Houve predomínio masculino (relação 2:1). Quando comparados ao grupo com EM, os pacientes MOG-IgG positivos apresentam idade mais avançada (mediana de 47 anos) e tiveram uma frequência maior de NO bilateral e/ou recorrente. Todos os pacientes com EM foram negativos para MOG-IgG (ensaio baseado em células). Materias e métodos: De um total de 38 pacientes com neuropatia óptica, seis foram MOG-IgG positivos e oito preencheram critérios diagnósticos para EM. Comparamos os nossos pacientes com NO MOG-IgG positivos com pacientes com NO associada a esclerose múltipla (EM). Optic neuritis multiple sclerosis myelin oligodendrocyte glycoprotein autoantibodies demyelinating diseasesĪutoanticorpos contra a glicoproteína da mielina do oligodendrócito (MOG-IgG) têm sido descritos em pacientes com neurite óptica (NO) isolada, entre outras doenças inflamatórias do sistema nervoso central. Conclusion: These findings suggest that MOG-IgG is a biomarker of an inflammatory demyelinating CNS disease distinct from MS. The brain magnetic resonance imaging of all MOG-IgG positive patients was normal or had only unspecific white matter T2 lesions. When compared with the MS group, the MOG-IgG patients were older (mean 47 years), more frequently male (ratio 2:1) and had a higher frequency of bilateral and/or recurrent ON.

All MS patients were negative for MOG-IgG using a cell-based assay.

Methods and results: Among the total of 38 patients with optic neuropathies, six patients with isolated ON were MOG-IgG positive and eight patients with ON fulfilled the diagnostic criteria for MS. We compared our MOG-IgG ON patients with multiple sclerosis (MS) patients presenting with ON. Pontifícia Universidade Católica do Rio Grande do Sul, Faculdade de Medicina, Hospital São Lucas, Serviço de Neurologia, Porto Alegre RS, BrasilInstituto do Cérebro do Rio Grande do Sul, Porto Alegre RS, Brasil Douglas Kazutoshi SatoĪutoantibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) have been reported in patients with inflammatory central nervous system disorders including isolated optic neuritis (ON). Pontifícia Universidade Católica do Rio Grande do Sul, Faculdade de Medicina, Hospital São Lucas, Serviço de Neurologia, Porto Alegre RS, BrasilInstituto do Cérebro do Rio Grande do Sul, Porto Alegre RS, Brasilīoth authors contributed equally to this work.
