Frequency of myelin oligodendrocyte glycoprotein antibody in multiple sclerosis

Cobo‐Calvo, Álvaro; d’Indy, Hyacintha; Ruiz, Anne; Collongues, Nicolas; Kremer, Laurent; Durand‐Dubief, Françoise; Rollot, Fabien; Casey, Romain; Vukusic, Sandra; Sèze, Jérôme De; Marignier, Romain

doi:10.1212/nxi.0000000000000649

Cited by 57 publications

(52 citation statements)

References 10 publications

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“…The serologic detection of MOG-IgG is useful diagnostically and the features of the antibody may provide insight into pathogenesis. A recent large study of MOG antibodies in MS showed it is detected in only 0.2%, highlighting its utility in discriminating from MS [8]. While in our study we used two sites for MOG-IgG detection, our multi-center collaborative studies have shown the live-cell based MOG assay cut-offs show consistent results across centers for a non-MS phenotype [77].…”

Section: Discussionmentioning

confidence: 62%

The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody

et al. 2020

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We sought to define the pathological features of myelin oligodendrocyte glycoprotein (MOG) antibody associated disorders (MOGAD) in an archival autopsy/biopsy cohort. We histopathologically analyzed 2 autopsies and 22 brain biopsies from patients with CNS inflammatory demyelinating diseases seropositive for MOG-antibody by live-cell-based-assay with full length MOG in its conformational form. MOGAD autopsies (ages 52 and 67) demonstrate the full spectrum of histopathological features observed within the 22 brain biopsies (median age, 10 years; range, 1-66; 56% female). Clinical, radiologic, and laboratory characteristics and course (78% relapsing) are consistent with MOGAD. MOGAD pathology is dominated by coexistence of both perivenous and confluent white matter demyelination, with an over-representation of intracortical demyelinated lesions compared to typical MS. Radially expanding confluent slowly expanding smoldering lesions in the white matter as seen in MS, are not present. A CD4+ T-cell dominated inflammatory reaction with granulocytic infiltration predominates. Complement deposition is present in all active white matter lesions, but a preferential loss of MOG is not observed. AQP4 is preserved, with absence of dystrophic astrocytes, and variable oligodendrocyte and axonal destruction. MOGAD is pathologically distinguished from AQP4-IgG seropositive NMOSD, but shares some overlapping features with both MS and ADEM, suggesting a transitional pathology. Complement deposition in the absence of selective MOG protein loss suggest humoral mechanisms are involved, however argue against endocytic internalization of the MOG antigen. Parallels with MOG-EAE suggest MOG may be an amplification factor that augments CNS demyelination, possibly via complement mediated destruction of myelin or ADCC phagocytosis.

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Section: Discussionmentioning

confidence: 62%

The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody

et al. 2020

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“…138 The second study analysed serum samples from 685 consecutive patients with MS, and found only two of them (0.3%) were MOG-IgG positive. 139 Both studies clearly indicate that MOG-IgG is rare in MS and if present indicate either insufficient assay specificity or an inappropriate clinical diagnosis.…”

Section: Treatment and Outcomementioning

confidence: 99%

Recent developments in MOG-IgG associated neurological disorders

Hegen

Reindl

2020

Ther Adv Neurol Disord

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In the past few years, acquired demyelinating syndromes of the central nervous system associated with antibodies against myelin oligodendrocyte glycoprotein (MOG) have evolved into a new inflammatory disease entity distinct from neuromyelitis optica spectrum disorders or multiple sclerosis. The meticulous clinical description of patients with MOG IgG antibodies (MOG-IgG) has been achieved by development and use of highly specific cell-based assays. MOG-IgG associated disorders comprise a wide spectrum of syndromes ranging from acute disseminated encephalomyelitis predominantly in children to optic neuritis or myelitis mostly in adults. In recent studies, phenotype of MOG-IgG associated disorders has further broadened with the description of cases of brainstem encephalitis, encephalitis with seizures and overlap syndromes with other types of autoimmune encephalitis. In this review, we provide an overview of current knowledge of MOG-IgG associated disorders, describe the clinical presentations identified, highlight differences from neuromyelitis optica spectrum disorders and multiple sclerosis, summarize clinical outcome and concepts of immune treatment, depict the underlying mechanisms of antibody pathogenicity and provide the methodological essentials of MOG-IgG assays.

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“…The proof of serum autoantibodies directed against aquaporin-4 (AQP4-IgG) in around 80% of cases established NMOSD as a distinct disease from multiple sclerosis (MS) (7)(8)(9)(10). In a subgroup of AQP4-IgG negative NMOSD patients serum antibodies targeting the myelin oligodendrocyte glycoprotein (MOG-IgG) were detected (11)(12)(13)(14)(15)(16). MOG-IgG+ patients with clinical and neuroimaging characteristics of NMOSD are currently discussed as a different disease entity (17)(18)(19)(20)(21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

Differences in Advanced Magnetic Resonance Imaging in MOG-IgG and AQP4-IgG Seropositive Neuromyelitis Optica Spectrum Disorders: A Comparative Study

et al. 2020

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Aims: To explore differences in advanced brain magnetic resonance imaging (MRI) characteristics between myelin oligodendrocyte (MOG) immunoglobulin (IgG) and aquaporin-4 (AQP4) IgG seropositive (+) neuromyelitis optica spectrum disorders (NMOSD). Methods: 33 AQP4-IgG and 18 MOG-IgG seropositive NMOSD patients and 61 healthy control (HC) subjects were included. All 112 participants were scanned with the same standardized MRI-protocol on a 3-Tesla MRI-scanner. Brain volume and diffusion tensor imaging (DTI) parameters were assessed. Results: MOG-IgG+ patients showed reduced parallel diffusivity within white matter tracts compared to HC whereas AQP4-IgG+ showed no significant brain parenchymal damage in DTI analysis. AQP4-IgG+ patients showed reduced whole brain volumes and reduced volumes of several deep gray matter structures compared to HC whereas MOG-IgG+ patients did not show reduced brain or deep gray matter volumes compared to HC. Conclusions: Microstructural brain parenchymal damage in MOG-IgG+ patients was more pronounced than in AQP4-IgG+ patients, compared with HC, whereas normalized brain volume reduction was more severe in AQP4-IgG+ patients. Longitudinal imaging studies are warranted to further investigate this trend in NMOSD. Our results suggest Schmidt et al. MRI Differences in NMOSD that MOG-IgG+ and AQP4-IgG+ NMOSD patients differ in cerebral MRI characteristics. Advanced MRI analysis did not help to differentiate between MOG-IgG+ and AQP4-IgG+ patients in our study.

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Frequency of myelin oligodendrocyte glycoprotein antibody in multiple sclerosis

Cited by 57 publications

References 10 publications

The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody

The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody

Recent developments in MOG-IgG associated neurological disorders

Differences in Advanced Magnetic Resonance Imaging in MOG-IgG and AQP4-IgG Seropositive Neuromyelitis Optica Spectrum Disorders: A Comparative Study

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