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J Neuroinflammation. 2016 Sep 26;13(1):279.

MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 1: Frequency, syndrome specificity, influence of disease activity, long-term course, association with AQP4-IgG, and origin.

Author information

Molecular Neuroimmunology Group, Otto Meyerhof Center, Department of Neurology, University Hospital Heidelberg, Im Neuenheimer Feld 350, 69120, Heidelberg, Germany.
Department of Neurology, Charité-University Medicine Berlin, Berlin, Germany.
Department of Neurology, Ruhr University Bochum, Bochum, Germany.
NeuroCure Clinical Research Center and Clinical and Experimental Multiple Sclerosis Research Center, Department of Neurology, Charité University Medicine, Berlin, Germany.
Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine, Charité University Medicine Berlin, Berlin, Germany.
Department of Neurology and Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.
Department of Neurology, Albert Ludwigs University, Freiburg, Germany.
Department of Neurology, Hannover Medical School, Hannover, Germany.
Department of Neurology, Heinrich Heine University, Düsseldorf, Germany.
Department of Neurology, University of Rostock, Rostock, Germany.
Department of Neurology, Julius Maximilians University, Würzburg, Germany.
Molecular Neuroimmunology Group, Otto Meyerhof Center, Department of Neurology, University Hospital Heidelberg, Im Neuenheimer Feld 350, 69120, Heidelberg, Germany.
IRCCS, C. Mondino National Neurological Institute, Pavia, Italy.
Centro di Riferimento Regionale SM, Azienda Ospedaliero Universitaria San Luigi Gonzaga, Orbassano, Italy.
Department of Clinical Immunology, Odense University Hospital, Odense, Denmark.
Institute of Experimental Immunology, affiliated to Euroimmun AG, Lübeck, Germany.
Clinical Department of Neurology, Medical University Innsbruck, Innsbruck, Austria.



Antibodies to myelin oligodendrocyte glycoprotein (MOG-IgG) have been suggested to play a role in a subset of patients with neuromyelitis optica and related disorders.


To assess (i) the frequency of MOG-IgG in a large and predominantly Caucasian cohort of patients with optic neuritis (ON) and/or myelitis; (ii) the frequency of MOG-IgG among AQP4-IgG-positive patients and vice versa; (iii) the origin and frequency of MOG-IgG in the cerebrospinal fluid (CSF); (iv) the presence of MOG-IgG at disease onset; and (v) the influence of disease activity and treatment status on MOG-IgG titers.


614 serum samples from patients with ON and/or myelitis and from controls, including 92 follow-up samples from 55 subjects, and 18 CSF samples were tested for MOG-IgG using a live cell-based assay (CBA) employing full-length human MOG-transfected HEK293A cells.


MOG-IgG was detected in 95 sera from 50 patients with ON and/or myelitis, including 22/54 (40.7 %) patients with a history of both ON and myelitis, 22/103 (21.4 %) with a history of ON but no myelitis and 6/45 (13.3 %) with a history of longitudinally extensive transverse myelitis but no ON, and in 1 control patient with encephalitis and a connective tissue disorder, all of whom were negative for AQP4-IgG. MOG-IgG was absent in 221 further controls, including 83 patients with AQP4-IgG-seropositive neuromyelitis optica spectrum disorders and 85 with multiple sclerosis (MS). MOG-IgG was found in 12/18 (67 %) CSF samples from MOG-IgG-seropositive patients; the MOG-IgG-specific antibody index was negative in all cases, indicating a predominantly peripheral origin of CSF MOG-IgG. Serum and CSF MOG-IgG belonged to the complement-activating IgG1 subclass. MOG-IgG was present already at disease onset. The antibodies remained detectable in 40/45 (89 %) follow-up samples obtained over a median period of 16.5 months (range 0-123). Serum titers were higher during attacks than during remission (p < 0.0001), highest during attacks of simultaneous myelitis and ON, lowest during acute isolated ON, and declined following treatment.


To date, this is the largest cohort studied for IgG to human full-length MOG by means of an up-to-date CBA. MOG-IgG is present in a substantial subset of patients with ON and/or myelitis, but not in classical MS. Co-existence of MOG-IgG and AQP4-IgG is highly uncommon. CSF MOG-IgG is of extrathecal origin. Serum MOG-IgG is present already at disease onset and remains detectable in the long-term course. Serum titers depend on disease activity and treatment status.


Antibody index; Aquaporin-4 antibodies (AQP4-IgG); Autoantibodies; Cell-based assays; Cerebrospinal fluid; Devic’s syndrome; Longitudinally extensive transverse myelitis (LETM); Multiple sclerosis; Myelin oligodendrocyte glycoprotein antibodies (MOG-IgG); Neuromyelitis optica antibodies (NMO-IgG); Neuromyelitis optica spectrum disorders (NMOSD); Neuromyelitis optica (NMO); Optic neuritis; Transverse Myelitis

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