Antibody responses to EBV and native MOG in pediatric inflammatory demyelinating CNS diseases

Selter, Rebecca C; Brilot, Fabienne; Grummel, Verena; Kraus, Verena; Cepok, Sabine; Dale, Russell C.; Hemmer, Bernhard

doi:10.1212/wnl.0b013e3181e04096

Cited by 52 publications

(33 citation statements)

References 10 publications

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“…All studies analyzing anti-MOG reactivity in pediatric patients noted a higher reactivity in young children (age <10 years) [Brilot et al 2009;McLaughlin et al 2009;Probstel et al 2011]. No linkage between anti-MOG and anti-Epstein-Barr virus (EBV) antibodies was seen [Selter et al 2010]. Cells transfected with hMOG are significantly more prone to natural killer (NK)-mediated cytotoxicity after incubation with purified serum IgG from anti-MOG positive patients, as compared with IgG from anti-MOG negative patients [Brilot et al 2009].…”

Section: Anti-mog Antibodies In a Proportion Of Pediatric Ms And Ademmentioning

confidence: 99%

Glycoproteins as targets of autoantibodies in CNS inflammation: MOG and more

Mayer

Meinl

2012

Ther Adv Neurol Disord

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Lessons from animal models MOG can be involved in CNS autoimmunity in principally two different ways. First, MOGspecific T cells evoke CNS inflammation. Second, anti-MOG antibodies lead to the induction of demyelination. Demyelination is a characteristic feature of MS lesions indicated by the presence of naked demyelinated axons. Glycoproteins as targets of autoantibodies in CNS inflammation: MOG and more Marie Cathrin Mayer and Edgar MeinlAbstract: B cells and antibodies constitute an important element in different inflammatory diseases of the central nervous system (CNS). Autoantibodies can serve as a biomarker to identify disease subgroups and may in addition contribute to the pathogenic process. One candidate autoantigen for multiple sclerosis (MS) is myelin oligodendrocyte glycoprotein (MOG). MOG is localized at the outermost surface of myelin in the CNS and has been the focus of extensive research for more than 30 years. Its role as an important autoantigen for T cells and as a target of demyelinating autoantibodies has been established in several variants of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. The literature regarding antibodies to MOG in MS patients is confusing and contradictory. Recent studies, however, have described high levels of antibodies to conformationally correct MOG in pediatric acquired demyelination, both acute disseminated encephalomyelitis (ADEM) and MS. In adult MS, such antibodies are rarely found and then only at low levels. In this review, we summarize key findings from animal models and patient studies, discuss challenges in detecting anti-MOG antibodies in patients and present recent approaches to identifying new autoantigens in MS.

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Section: Anti-mog Antibodies In a Proportion Of Pediatric Ms And Ademmentioning

confidence: 99%

Glycoproteins as targets of autoantibodies in CNS inflammation: MOG and more

Mayer

Meinl

2012

Ther Adv Neurol Disord

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“…As well as MS, these findings are also applicable to neuromyelitis optica and acute demyelinating encephalomyelitis, where people also have significant levels of antibodies to MOG and in particular responses to native MOG. 23,24 Initial studies describing the encephalitogenic potential of MOG 35-55 made use of the human MOG sequences 10 whereas later studies reported the pathogenic potential of mouse sequences. In the initial studies the search for encephalitogenic epitopes was not performed systematically as we have reported for Biozzi ABH and SJL mice.…”

Section: Discussionmentioning

confidence: 99%

Novel pathogenic epitopes of myelin oligodendrocyte glycoprotein induce experimental autoimmune encephalomyelitis in C57BL/6 mice

et al. 2013

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SummaryMyelin oligodendrocyte glycoprotein (MOG), a minor protein of the central nervous system myelin, is recognized as a potential target in multiple sclerosis and neuromyelitis optica. The extracellular domain of MOG is commonly used in a wide range of mouse strains and other animals to induce experimental autoimmune encephalomyelitis (EAE), an autoimmune animal model of multiple sclerosis, because it is a target for antibody-mediated attack. Previous studies, using selected peptides, have indicated that MOG peptide is an encephalitogenic epitope in C57BL/ , MOG 120-134 (localized in the transmembrane region) and MOG [183][184][185][186][187][188][189][190][191][192][193][194][195][196][197] (in the second hydrophobic MOG domain). In addition, residue MOG 113-127 was found to be a B-cell epitope, suggesting that this may be a useful adjunct for the induction of EAE as well as for immunological studies in C57BL/6 mice, which are increasingly being used to study immune function through the use of transgenic and gene knockout technology.

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“…All studies analyzing anti-MOG reactivity in pediatric patients noted a higher reactivity in young children (age b 10 years) [27,31,32]. No linkage between anti-MOG and anti-EBV antibodies was seen [34]. Cells transfected with hMOG are significantly more prone to NK-mediated cytotoxicity after incubation with purified serum IgG from anti-MOG positive patients, as compared to IgG from anti-MOG negative patients [27].…”

Section: Anti-mog Antibodies In Pediatric Ms and Ademmentioning

confidence: 98%

Viability of autoantibody-targets: How to tackle pathogenetic heterogeneity as an obstacle for treatment of multiple sclerosis

Mayer¹,

Hohlfeld²,

Meinl³

2012

Journal of the Neurological Sciences

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Antibody responses to EBV and native MOG in pediatric inflammatory demyelinating CNS diseases

Abstract: High serum immunoglobulin G titers to native myelin oligodendrocyte glycoprotein are found in a significant number of children affected by clinically isolated syndrome or acute disseminated encephalomyelitis. These antibodies are not related to the antibody response to Epstein-Barr virus.

Cited by 52 publications

References 10 publications

Glycoproteins as targets of autoantibodies in CNS inflammation: MOG and more

Glycoproteins as targets of autoantibodies in CNS inflammation: MOG and more

Novel pathogenic epitopes of myelin oligodendrocyte glycoprotein induce experimental autoimmune encephalomyelitis in C57BL/6 mice

Viability of autoantibody-targets: How to tackle pathogenetic heterogeneity as an obstacle for treatment of multiple sclerosis

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