Review Article | Published:

The spectrum of MOG autoantibody-associated demyelinating diseases

Nature Reviews Neurology volume 9, pages 455461 (2013) | Download Citation

Abstract

Myelin oligodendrocyte glycoprotein (MOG) has been identified as a target of demyelinating autoantibodies in animal models of inflammatory demyelinating diseases of the CNS, such as multiple sclerosis (MS). Numerous studies have aimed to establish a role for MOG antibodies in patients with MS, although the results have been controversial. Cell-based immunoassays using MOG expressed in mammalian cells have demonstrated the presence of high-titre MOG antibodies in paediatric patients with acute disseminated encephalomyelitis, MS, aquaporin-4-seronegative neuromyelitis optica, or isolated optic neuritis or transverse myelitis, but only rarely in adults with these disorders. These studies indicate that MOG antibodies could be associated with a broad spectrum of acquired human CNS demyelinating diseases. This Review article discusses the current literature on MOG antibodies, their potential clinical relevance, and their role in the pathogenesis of MOG antibody-associated demyelinating disorders.

Key points

  • Myelin oligodendrocyte glycoprotein (MOG) is a target of demyelinating autoantibodies in animal models of inflammatory demyelinating diseases of the CNS

  • Studies using cell-based immunoassays have identified MOG antibodies in human inflammatory demyelinating CNS diseases

  • High-titre MOG antibodies are present in paediatric patients with acute disseminated encephalomyelitis, multiple sclerosis (MS), aquaporin-4-seronegative neuromyelitis optica, or isolated optic neuritis or transverse myelitis

  • High-titre MOG antibodies are only rarely seen in adults with these demyelinating CNS disorders

  • MOG antibodies might be associated with a broad spectrum of acquired human CNS demyelinating diseases

  • The clinical presentation observed in anti-MOG-positive patients resembles the disease features in experimental animal models more closely than the clinical presentation of patients with MS

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Acknowledgements

The authors' research is funded by grants W1206 and I916 from the Austrian Science Fund (FWF; M. Reindl) and grant 14158 from the Jubilaeumsfonds of the Austrian National Bank (K. Rostásy).

Author information

Affiliations

  1. Clinical Department of Neurology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria

    • Markus Reindl
    • , Franziska Di Pauli
    •  & Thomas Berger
  2.  Department of Pediatrics I, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria

    • Kevin Rostásy

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Contributions

M. Reindl, F. Di Pauli, K. Rostásy and T. Berger contributed equally to researching data for the article, discussion of the content, writing, and review and/or editing of the manuscript before submission.

Competing interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to Markus Reindl.

Supplementary information

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    Supplementary Table 1

    A comparison of methods using human MOG expressed in mammalian cells for the detection of serum MOG-IgG

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DOI

https://doi.org/10.1038/nrneurol.2013.118

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