Detection of MOG-IgG in Clinical Samples by Live Cell-Based Assays: Performance of Immunofluorescence Microscopy and Flow Cytometry

Marchionatti, Amanda; Hansel, Gisele; Ávila, Gabriela Urbanski; Sato, Douglas Kazutoshi

doi:10.3389/fimmu.2021.642272

Cited by 4 publications

(3 citation statements)

References 27 publications

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“…It was found that the titre value of MOG-Ab in the serum of the patients varied greatly, which can be used to predict relapse (Tea et al, 2019;Marchionatti et al, 2021), supporting the pathogenic role of MOG-Ab. However, the MOG-Ab titre value was not entirely positively correlated with the severity and recurrence of the patient's disease in our study, which may be related to the timing of serum collection, meaning that the titre value will decrease significantly after steroid therapy.…”

Section: Discussionmentioning

confidence: 86%

Myelin Oligodendrocyte Glycoprotein Antibody Associated Cerebral Cortical Encephalitis: Case Reports and Review of Literature

Shu

Ding

Shang

et al. 2022

Front. Hum. Neurosci.

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Myelin oligodendrocyte glycoprotein antibody-associated disease is an immune-mediated demyelinating disease of the central nervous system that is present in both adults and children. The most common clinical manifestations are optic neuritis, myelitis, acute disseminated encephalomyelitis, and brainstem syndrome. Cerebral cortical encephalitis (CCE) is a rare clinical phenotype of myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD), which usually begins with seizures, headaches, and fever, and may be misdiagnosed as viral encephalitis in the early stages. Herein, we report two typical MOG antibody (MOG-Ab)-positive patients presenting with CCE, both of whom presented with headache, fever, seizures, and who recovered completely after immunotherapy. In addition, we performed a systematic review of the present literature from the perspectives of population characteristics, clinical symptoms, MRI abnormalities, treatments, and prognosis. Among the patients reported in 25 articles, 33 met our inclusion criteria, with the age of onset ranging from 4 to 52 years. Most of the patients had seizures, headache, fever, and unilateral cortical lesions on brain MRI. For acute CCE, 30 patients were treated with high-dose intravenous methylprednisolone, and the symptoms of most patients were completely relieved after immunotherapy. This study reported our experience and lessons learned in the diagnosis and treatment of MOG-Ab-positive CCE and provides a systematic review of the literature to analyse this rare clinical phenotype.

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Section: Discussionmentioning

confidence: 86%

Myelin Oligodendrocyte Glycoprotein Antibody Associated Cerebral Cortical Encephalitis: Case Reports and Review of Literature

Shu

Ding

Shang

et al. 2022

Front. Hum. Neurosci.

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“…Patient serum samples are incubated with live HEK293 cells expressing fulllength MOG protein on their membrane, followed by secondary staining with anti-human IgG (H+L or Fc) or IgG1 (Fc) secondary antibodies. The analysis is done either by immune fluorescence microscopy or flow cytometry (35,36).…”

Section: Anti-mog Iggmentioning

confidence: 99%

Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease

Corbali

Chitnis

2023

Front. Neurol.

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Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is a spectrum of diseases, including optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cerebral cortical encephalitis. In addition to distinct clinical, radiological, and immunological features, the infectious prodrome is more commonly reported in MOGAD (37–70%) than NMOSD (15–35%). Interestingly, pediatric MOGAD is not more aggressive than adult-onset MOGAD, unlike in multiple sclerosis (MS), where annualized relapse rates are three times higher in pediatric-onset MS. MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross blood brain barrier (BBB). MOGAD lesions show a perivenous confluent pattern around the small veins, lacking the radiological central vein sign. Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden antigen-presenting cells and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. CD4+ T cells, unlike CD8+ T cells in MS, are the dominant T cell type found in lesion histology. Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses. MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. Stimulation of peripheral MOG-specific B cells through TLR stimulation or T follicular helper cells might help differentiate MOG antibody-producing plasma cells in the peripheral blood. Neuroinflammatory biomarkers (such as MBP, sNFL, GFAP, Tau) in MOGAD support that most axonal damage happens in the initial attack, whereas relapses are associated with increased myelin damage.

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“…Therefore, CBA is widely used for the detection of these autoantibodies and can maintain conformational epitopes through transfected cells expressing natively folded proteins [7]. The CBA can be carried out using either indirect immunofluorescence microscopy (IIF) or flow cytometry methods; CBA using IIF is widely used but is semi-quantitative, but CBA by flow cytometry is an automated method with quantification that reduces human bias [8]. And when the CBA is performed in-house, it requires the genetic information of antigenic epitope, transfected cell culture, and skilled analysis of cytochemical staining results, all of which affect the accuracy of the test and limit its application in clinical diagnosis.…”

Section: Detection Of Autoantibodiesmentioning

confidence: 99%

Autoantibodies in central nervous system and neuromuscular autoimmune disorders: A narrative review

et al. 2022

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The discovery of novel autoantibodies in neurological disorders contributes to a better understanding of its pathogenesis, improves the accuracy of diagnosis, and leads to new treatment strategies. Advances in techniques for the screening and detection of autoantibodies have enabled the discovery of new antibodies in the central nervous system (CNS) and neuromuscular diseases. Cell-based assays using live or fixed cells overexpressing target antigens are widely used for autoantibody-based diagnosis in clinical practice. Common pathogenic autoantibodies are unknown in most patients with multiple sclerosis (MS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Novel pathogenic autoantibodies to aquaporin-4 and myelin oligodendrocyte glycoprotein (MOG) have been identified in neuromyelitis optica spectrum disorder and MOG antibody-associated disease, respectively. These diseases have clinical similarities to MS, but with the discovery of pathogenic autoantibodies, they are now recognized as distinct disease entities. Antibodies to paranodal membrane proteins such as neurofascin-155, contactin‑1, contactin‑associated protein‑1 in CIDP and muscle-specific kinase and low-density lipoprotein receptor–related protein 4 in myasthenia gravis were added to the profiles of autoantibodies in neurological disorders. Despite the relatively low frequency of seropositivity, autoantibody detection is currently essential for the clinical diagnosis of CNS and neuromuscular autoimmune disorders, and differential approaches to seropositive patients will contribute to more personalized medicine. We reviewed recent discoveries of autoantibodies and their clinical implications in CNS and neuromuscular disorders.

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Detection of MOG-IgG in Clinical Samples by Live Cell-Based Assays: Performance of Immunofluorescence Microscopy and Flow Cytometry

Cited by 4 publications

References 27 publications

Myelin Oligodendrocyte Glycoprotein Antibody Associated Cerebral Cortical Encephalitis: Case Reports and Review of Literature

Myelin Oligodendrocyte Glycoprotein Antibody Associated Cerebral Cortical Encephalitis: Case Reports and Review of Literature

Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease

Autoantibodies in central nervous system and neuromuscular autoimmune disorders: A narrative review

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