Neuropediatrics 2011; 42 - P049
DOI: 10.1055/s-0031-1274021

Anti-MOG autoantibodies in children with acute demyelination: Comparison of assays and longitudinal analysis

AK Pröbstel 1, 2, K Dornmair 1, 2, R Bittner 1, 2, P Sperl 1, 2, D Jenne 1, S Magalhaes 3, A Villalobos 3, C Breithaupt 4, R Weissert 5, U Jacob 6, M Krumbholz 1, 2, T Kümpfel 2, A Blaschek 7, W Stark 8, J Gärtner 8, D Pohl 9, K Rostasy 10, F Weber 11, I Forne 12, M Khademi 13, T Olsson 13, F Brilot 14, E Tantsis 14, RC Dale 14, H Wekerle 1, R Hohlfeld 1, 2, B Banwell 15, A Bar-Or 3, E Meinl 1, 2, T Derfuß 16
  • 1Max-Planck-Institut für Neurobiologie, Abt. Neuroimmunologie, Martinsried, Germany
  • 2Ludwig-Maximilians-Universität München, Klinikum Großhadern, Klinische Neuroimmunologie, München, Germany
  • 3Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Canada
  • 4Institute of Biochemistry and Biotechnology, Martin-Luther-University Halle-Wittenberg, Halle, Germany
  • 5Department of Neurology, University of Geneva Hospital, Geneva, Switzerland
  • 6Westend-Innovation, Biotech Consulting, München, Germany
  • 7Department of Pediatric Neurology and Developmental Medicine, Dr von Haunersches Kinderspital, Ludwig-Maximilians-University, München, Germany
  • 8Department of Pediatrics and Pediatric Neurology, Georg August University, Göttingen, Germany
  • 9Children's Hospital of Eastern Ontario, Ottawa, Canada
  • 10Division of Neuropediatrics and Inherited Metabolic Disorders, Department of Pediatrics, Innsbruck Medical University, Innsbruck, Austria
  • 11RG Inflammatory disorders of the Central Nervous System, Max Planck Institute of Psychiatry, München, Germany
  • 12Munich Centre of Integrated Protein Science and Adolf Butenandt Institute, Ludwig-Maximilians-University, München, Germany
  • 13Neuroimmunology Unit, Department of Clinical Neuroscience, Karolinska University Hospital, Stockholm, Sweden
  • 14Neuroinflammation group, Institute of Neuroscience and Muscle Research, the Kids Research Institute at the Children's Hospital at Westmead, University of Sydney, Sydney, Australia
  • 15Division of Neurology, Department of Paediatrics, The Hospital for Sick Children, Toronto, Canada
  • 16Department of Neurology, University Hospital Basel, Basel, Switzerland

Aims: Myelin oligodendrocyte glycoprotein (MOG) is a target of demyelinating antibodies in several species. Anti-MOG IgG are found in a proportion of children with acute central nervous system demyelinating disease, but the long-term kinetic of anti-MOG autoantibodies is unknown.

Methods: For detection of anti-MOG antibodies two different methods were compared: Western blot with purified myelin and grey matter glycoproteins and flow cytometry with MOG-transfected cells. We addressed the presence of serum anti-MOG Ig in a cross-sectional study analyzing 126 pediatric patients with acute demyelination and 64 adult patients with multiple sclerosis (MS). This was supplemented by a prospective study comprising 77 pediatric patients.

Results: The cross-sectional part of our study elaborated that MOG-transfected cells were recognized by 25% of children with acute demyelination, but by none of the pediatric or adult controls. Sera from 4/64 (6%) adult MS patients had anti-MOG IgG at low levels. Antibodies to MOG were mainly IgG1 and their binding was largely blocked by pathogenic anti-MOG antibodies derived from a spontaneous animal model of autoimmune encephalitis. In contrast, the Western blot did not distinguish between patients and controls. In the prospective part of our study, twenty-five children who were anti-MOG Ig positive at disease onset were followed for up to five years. Anti-MOG antibodies rapidly and continuously declined in all 16 monophasic patients with acute disseminated encephalomyelitis (ADEM) and in one patient with clinically isolated syndrome (CIS). In contrast, in 6 of 8 patients (75%) eventually diagnosed with childhood MS the antibodies to MOG persisted with fluctuations showing a second increase during an observation period of up to 5 years.

Conclusions: The persistence or disappearance of antibodies to MOG may have prognostic relevance for acute childhood demyelination.