Anti-MOG antibodies in adult patients with demyelinating disorders of the central nervous system

Tanaka, Masami; Tanaka, Keiko

doi:10.1016/j.jneuroim.2014.03.001

Cited by 56 publications

(55 citation statements)

References 17 publications

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“…Our results are contradictory to those in several recent reports, in which MOG-ab was found only in AQP4-ab seronegative NMOSD patients (Kitley et al, 2014; Kitley et al, 2012; Mader et al, 2011; Rostasy et al, 2013; Sato et al, 2014; Tanaka and Tanaka, 2014). However, others noted one double-positive patient among 20 with NMOSD (Kezuka et al, 2012).…”

Section: Discussioncontrasting

confidence: 99%

“…Kitley’s group published two papers on MOG-ab detection (Rostasy et al, 2013; Mader et al, 2011; Kitley et al, 2012, 2014), but they also used C-terminal-truncated MOG-EGFP fusion genes, which detect only antibodies on the cell surface. Tanaka and Sato used full-length MOG transiently transfected HEK 293 cells for MOG-ab detection (Sato et al, 2014; Tanaka and Tanaka, 2014), but Tanaka’s team transfected MOG only, and the Sato group transfected a MOG-IRES-DsRed cassette. Both of these constructs lack signals for the efficient monitoring of MOG expression.…”

Section: Discussionmentioning

confidence: 99%

“…The presence of antibodies against MOG revealed in several recent studies suggests that this could be the case (Kitley et al, 2014; Kitley et al, 2012; Mader et al, 2011; Rostasy et al, 2013; Sato et al, 2014; Tanaka and Tanaka, 2014). Although MOG autoantibodies (MOG-ab) were identified in NMOSD and later confirmed in six independent studies (Kitley et al, 2014; Kitley et al, 2012; Mader et al, 2011; Rostasy et al, 2013; Sato et al, 2014; Tanaka and Tanaka, 2014), whether NMOSD patients can carry antibodies to both AQP4 and MOG remains controversial (Kezuka et al, 2012; Kitley et al, 2014; Weinshenker and Wingerchuk, 2014; Woodhall et al, 2013). If so, do they exhibit any unique clinical characteristics?…”

Section: Introductionmentioning

confidence: 97%

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Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD

Yan

et al. 2016

Sci. China Life Sci.

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We characterized a unique group of patients with neuromyelitis optica spectrum disorder (NMOSD) who carried autoantibodies of aquaporin-4 (AQP4) and myelin-oligodendrocyte glycoprotein (MOG). Among the 125 NMOSD patients, 10 (8.0%) were AQP4-and MOG-ab double positive, and 14 (11.2%) were MOG-ab single positive. The double-positive patients had a multiphase disease course with a high annual relapse rate (P=0.0431), and severe residual disability (P<0.0001). Of the double-positive patients, 70% had MS-like brain lesions, more severe edematous, multifocal regions on spinal magnetic resonance imaging (MRI), pronounced decreases of retinal nerve fiber layer thickness and atrophy of optic nerves. In contrast, patients with only MOG-ab had a higher ratio of monophasic disease course and mild residual disability. Spinal cord MRI illustrated multifocal cord lesions with mild edema, and brain MRIs showed more lesions around lateral ventricles. NMOSD patients carrying both autoantibodies to AQP4 and MOG existed and exhibited combined features of prototypic NMO and relapsing-remitting form of MS, whereas NMOSD with antibodies to MOG only exhibited an "intermediate" phenotype between NMOSD and MS. Our study suggests that antibodies against MOG might be pathogenic in NMOSD patients and that determination of anti-MOG antibodies maybe instructive for management of NMOSD patients. MOG antibody, AQP4 antibody, neuromyelitis optica spectrum disorder, phenotypeCitation:

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD

Yan

et al. 2016

Sci. China Life Sci.

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“…11 A fulllength human MOG cDNA expression vector (a kind gift from Dr. M. Reindl, Innsbruck Medical University, Innsbruck, Austria) was transfected into human embryonic kidney (HEK) 293 cells using Lipofectamine reagent (Invitrogen Japan, Tokyo, Japan). Cell cultures were maintained in Dulbecco's modified Eagle's medium supplemented with 10% fetal calf serum.…”

Section: Antibody Assaysmentioning

confidence: 99%

Clinical Profile of Anti-Myelin Oligodendrocyte Glycoprotein Antibody Seropositive Cases of Optic Neuritis

Matsuda

Kezuka

Umazume

et al. 2015

Neuro-Ophthalmology

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We have studied the clinical picture of anti-aquaporin antibody (AQP4-Ab)-and anti-myelin oligodendrocyte glycoprotein antibody (MOG-Ab)-positive optic neuritis. However, optic neuritis associated with MOG-Abs has not been elucidated using new methods such as cell-based assay. Hence, we conducted a comprehensive investigation on its clinical profile. Serum samples from 70 patients (17 males and 53 females, mean age 43.1 years) with optic neuritis were tested for MOG-Abs by cell-based assay. In MOG-Ab seropositive patients, the disease type, recurrence status, and visual function outcome were analysed. Among 70 patients, 18 were MOGAb seropositive. The 18 patients comprised 2 with chronic relapsing inflammatory optic neuropathy, 2 with AQP4-Ab seropositive optic neuritis (neuromyelitis optica), 12 with idiopathic optic neuritis, and 2 with optic neuritis associated with multiple sclerosis. Excluding two cases that were also AQP4-Ab seropositive, MOG-Ab seropositive cases had relatively favourable visual acuity outcome (although not significantly different from seronegative cases) but had significant residual visual field deficit (p = 0.0015). Furthermore, the number of relapses of optic neuritis per year was significantly greater in MOG-Ab seropositive cases than in seronegative cases (0.82 vs. 0.40; p = 0.0005). MOG-Abs may contribute to the heterogeneous clinical picture of optic neuritis, and although visual acuity outcome is favourable, there is a tendency of residual visual field deficit and a possibility of repeated relapses.

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“…Accordingly, MOG-IgG-related NMO is now considered by many as a disease entity in its own right, immunopathogenetically distinct from its AQP4-IgG-positive counterpart. However, the cohorts included in previous clinical studies were relatively small (median 9 patients in [10–17, 22–24]) and the observation periods often short (median 24 months in [11–13, 15–17, 23–26]). Moreover, some previous studies did not, or not predominantly, include Caucasian patients [12, 15, 26], which is potentially important since genetic factors are thought to play a role in NMO [27].…”

Section: Introductionmentioning

confidence: 99%

MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome

Jarius

Ruprecht

Kleiter

et al. 2016

J Neuroinflammation

767

959

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Background: A subset of patients with neuromyelitis optica spectrum disorders (NMOSD) has been shown to be seropositive for myelin oligodendrocyte glycoprotein antibodies (MOG-IgG).Objective: To describe the epidemiological, clinical, radiological, cerebrospinal fluid (CSF), and electrophysiological features of a large cohort of MOG-IgG-positive patients with optic neuritis (ON) and/or myelitis (n = 50) as well as attack and long-term treatment outcomes.Methods: Retrospective multicenter study. Results: The sex ratio was 1:2.8 (m:f). Median age at onset was 31 years (range 6-70). The disease followed a multiphasic course in 80% (median time-to-first-relapse 5 months; annualized relapse rate 0.92) and resulted in significant disability in 40% (mean follow-up 75 ± 46.5 months), with severe visual impairment or functional blindness (36%) and markedly impaired ambulation due to paresis or ataxia (25%) as the most common long-term sequelae. Functional blindness in one or both eyes was noted during at least one ON attack in around 70%. Perioptic enhancement was present in several patients. Besides acute tetra-/paraparesis, dysesthesia and pain were common in acute myelitis (70%). Longitudinally extensive spinal cord lesions were frequent, but short lesions occurred at least once in 44%. Fourty-one percent had a history of simultaneous ON and myelitis. Clinical or radiological involvement of the brain, brainstem, or cerebellum was present in 50%; extra-opticospinal symptoms included intractable nausea and vomiting and respiratory insufficiency (fatal in one). CSF pleocytosis (partly neutrophilic) was present in 70%, oligoclonal bands in only 13%, and blood-CSF-barrier dysfunction in 32%. Intravenous methylprednisolone (IVMP) and long-term immunosuppression were often effective; however, treatment failure leading to rapid accumulation of disability was noted in many patients as well as flare-ups after steroid withdrawal. Full recovery was achieved by plasma exchange in some cases, including after IVMP failure. Breakthrough attacks under azathioprine were linked to the drug-specific latency period and a lack of cotreatment with oral steroids. Methotrexate was effective in 5/6 patients. Interferon-beta was associated with ongoing or increasing disease activity. Rituximab and ofatumumab were effective in some patients. However, treatment with rituximab was followed by early relapses in several cases; end-of-dose relapses occurred 9-12 months after the first infusion. Coexisting autoimmunity was rare (9%). Wingerchuk's 2006 and 2015 criteria for NMO(SD) and Barkhof and McDonald criteria for multiple sclerosis (MS) were met by 28%, 32%, 15%, 33%, respectively; MS had been suspected in 36%. Disease onset or relapses were preceded by infection, vaccination, or pregnancy/delivery in several cases. Conclusion: Our findings from a predominantly Caucasian cohort strongly argue against the concept of MOG-IgG denoting a mild and usually monophasic variant of NMOSD. The predominantly relapsing and often severe disease course ...

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Anti-MOG antibodies in adult patients with demyelinating disorders of the central nervous system

Cited by 56 publications

References 17 publications

Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD

Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD

Clinical Profile of Anti-Myelin Oligodendrocyte Glycoprotein Antibody Seropositive Cases of Optic Neuritis

MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome

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