Transient MOG antibody seroconversion associated with immunomodulating therapy

Marc Pawlitzki; Christin Campe; Leoni Rolfes; Hans-Jochen Heinze; Frank Leypoldt; Klaus-Peter Wandinger; Markus Reindl; Brigitte Wildemann; Sven Jarius; Peter Körtvelyessy

doi:10.1016/j.msard.2019.101420

Transient MOG antibody seroconversion associated with immunomodulating therapy

Mult Scler Relat Disord. 2020 Jan:37:101420. doi: 10.1016/j.msard.2019.101420. Epub 2019 Sep 28.

Authors

Affiliations

¹ Department of Neurology, Otto-von-Guericke University, Leipziger Straße 44, 39120 Magdeburg, Germany; Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany. Electronic address: [email protected].
² Department of Neurology, Otto-von-Guericke University, Leipziger Straße 44, 39120 Magdeburg, Germany.
³ Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
⁴ Department of Neurology, Otto-von-Guericke University, Leipziger Straße 44, 39120 Magdeburg, Germany; Leibniz Institute, Otto-von-Guericke University, Leipziger Straße 44, 39120 Magdeburg, Germany.
⁵ Neuroimmunology, Institute of Clinical Chemistry, University Hospital Schleswig-Holstein, Kiel, Germany.
⁶ Neuroimmunology, Institute of Clinical Chemistry, University Hospital Schleswig-Holstein, Lübeck, Germany.
⁷ Clinical Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
⁸ Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany.
⁹ Department of Neurology, Otto-von-Guericke University, Leipziger Straße 44, 39120 Magdeburg, Germany; Charité-Universitätsmedizin Berlin, Department of Neurology, Germany; German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany; German Center for Neurodegenerative Diseases (DZNE), Berlin, Germany.

PMID: 32172994
DOI: 10.1016/j.msard.2019.101420

Abstract

Immunoglobulin G (IgG) autoantibodies targeting myelin oligodendrocyte glycoprotein (MOG) have recently been associated with autoimmune CNS demyelination. We present the case of a 35-year-old patient who was seronegative for MOG-IgG (as confirmed by means of three independent immunoassays) during two corticosteroid-responsive attacks of brainstem encephalitis and optic neuritis, respectively, but turned positive for MOG-IgG under treatment with interferon-beta (IFN-beta), which was commenced 6 months after onset of the first attack. MOG-IgG serum levels declined after therapy was switched to glatiramer acetate. The fact that seroconversion was first observed under treatment with IFN-beta is in accordance with previous evidence suggesting a role of IFN-beta in disease exacerbation in antibody-mediated disorders.

Publication types

Case Reports

MeSH terms

Adult
Aquaporin 4 / immunology
Autoantibodies / blood
Autoantibodies / pharmacology*
Encephalitis / complications
Encephalitis / drug therapy
Humans
Immunoglobulin G / blood
Immunomodulation / immunology*
Myelin-Oligodendrocyte Glycoprotein / immunology*
Neuromyelitis Optica / complications
Neuromyelitis Optica / diagnosis
Neuromyelitis Optica / drug therapy
Optic Neuritis / diagnosis
Optic Neuritis / immunology
Optic Neuritis / therapy*
Seroconversion / drug effects
Seroconversion / physiology*

Substances

Aquaporin 4
Autoantibodies
Immunoglobulin G
Myelin-Oligodendrocyte Glycoprotein