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Cited by 206Multiple Sclerosis Research StudiesAutoimmune Neurological Disorders and TreatmentsPeripheral Neuropathies and Disorders

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Autoantibodies to MOG in a distinct subgroup of adult multiple sclerosis

Open access
Spadaro, Melania, Gerdes, Lisa Ann, Krumbholz, Markus, Ertl-Wagner, Birgit, Thaler, Franziska Sabrina, Schuh, Elisabeth, Metz, Imke, Blaschek, Astrid, Dick, Andrea, Brück, Wolfgang, Hohlfeld, Reinhard, Meinl, Edgar, Kümpfel, Tania·2016·Neurology Neuroimmunology & Neuroinflammation
DOI 10.1212/nxi.0000000000000257PMC PMC4949775
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Abstract

OBJECTIVES: To evaluate the presence of antibodies to conformation-intact myelin oligodendrocyte glycoprotein (MOG) in a subgroup of adult patients with clinically definite multiple sclerosis (MS) preselected for a specific clinical phenotype including severe spinal cord, optic nerve, and brainstem involvement. METHODS: Antibodies to MOG were investigated using a cell-based assay in 3 groups of patients: 104 preselected patients with MS (group 1), 55 age- and sex-matched, otherwise unselected patients with MS (group 2), and in 22 brain-biopsied patients with demyelinating diseases of the CNS (n = 19 with MS), 4 of whom classified as MS type II (group 3). Recognized epitopes were identified with mutated variants of MOG. RESULTS: Antibodies to MOG were found in about 5% (5/104) of preselected adult patients with MS. In contrast, in groups 2 and 3, none of the patients tested positive for MOG antibodies. Patients with MS with antibodies to MOG predominantly manifested with concomitant severe brainstem and spinal cord involvement and had a severe disease course with high relapse rates and failure to several disease-modifying therapies. Three of them had been treated with plasma exchange with a favorable response. All anti-MOG-positive patients with MS showed typical MS lesions on brain MRI. Longitudinal analysis up to 9 years revealed fluctuations and reappearance of anti-MOG reactivity. Epitope mapping indicated interindividual heterogeneity, yet intraindividual stability of the antibody response. CONCLUSIONS: Antibodies to MOG can be found in a distinct subgroup of adult MS with a specific clinical phenotype and may indicate disease heterogeneity.

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Figure 1. Antibodies to MOG in a proportion of adult patients with MS (A) Sera from 3 groups of patients with MS were analyzed for anti-MOG reactivity. Group 1: patients with MS with a specific clinical phenotype, namely, with severe or recurrent myelitis and/or severe (visual acuity <0.5) or recurrent optic neuritis, and/or brainstem syndrome (n = 104). Group 2: unselected patients with MS matched for age and sex (n = 55). Group 3: biopsied patients (n = 22), 4 with MS type II pathology (empty triangles). The red line indicates the cutoff for anti-MOG positivity. Values shown for each anti-MOG IgG–positive patient represent the mean of 3 independent measurements using the first serum sample analyzed, which was 14, 16, 3, 18, and 9 years after disease onset for patients 1 through 5. (B, C) Clinical features, therapies, and longitudinal analysis of antibodies to MOG in patients 1 and 2. (D) Analysis of the epitope specificity of the MOG reactivity of the samples indicated with asterisks (*) in C. Reactivity of the serum samples diluted 1:50 to the indicated variants of hMOG and to mMOG is shown. Values obtained with wild-type hMOG were set as 100% and the other reactivities were calculated as described.22 Depicted are the mean values of 3 independent experiments ± SEM. DMF = dimethyl fumarate; DMT = disease-modifying therapy; EDSS = Expanded Disability Status Scale; FTY = fingolimod; GLAT = glatiramer acetate; hMOG = human myelin oligodendrocyte glycoprotein; IgG = immunoglobulin G; IVIG = IV immunoglobulins; MFI = mean fluorescence intensity; mMOG = mouse myelin oligodendrocyte glycoprotein; MOG = myelin oligodendrocyte glycoprotein; MS = multiple sclerosis; NAT = natalizumab; PLEX = plasma exchange; RX = rituximab.
Figure 1. Antibodies to MOG in a proportion of adult patients with MS (A) Sera from 3 groups of patients with MS were analyzed for anti-MOG reactivity. Group 1: patients with MS with a specific clinical phenotype, namely, with severe or recurrent myelitis and/or severe (visual acuity <0.5) or recurrent optic neuritis, and/or brainstem syndrome (n = 104). Group 2: unselected patients with MS matched for age and sex (n = 55). Group 3: biopsied patients (n = 22), 4 with MS type II pathology (empty triangles). The red line indicates the cutoff for anti-MOG positivity. Values shown for each anti-MOG IgG–positive patient represent the mean of 3 independent measurements using the first serum sample analyzed, which was 14, 16, 3, 18, and 9 years after disease onset for patients 1 through 5. (B, C) Clinical features, therapies, and longitudinal analysis of antibodies to MOG in patients 1 and 2. (D) Analysis of the epitope specificity of the MOG reactivity of the samples indicated with asterisks (*) in C. Reactivity of the serum samples diluted 1:50 to the indicated variants of hMOG and to mMOG is shown. Values obtained with wild-type hMOG were set as 100% and the other reactivities were calculated as described.22 Depicted are the mean values of 3 independent experiments ± SEM. DMF = dimethyl fumarate; DMT = disease-modifying therapy; EDSS = Expanded Disability Status Scale; FTY = fingolimod; GLAT = glatiramer acetate; hMOG = human myelin oligodendrocyte glycoprotein; IgG = immunoglobulin G; IVIG = IV immunoglobulins; MFI = mean fluorescence intensity; mMOG = mouse myelin oligodendrocyte glycoprotein; MOG = myelin oligodendrocyte glycoprotein; MS = multiple sclerosis; NAT = natalizumab; PLEX = plasma exchange; RX = rituximab.CC BY-NC-ND · PubMed Central
Figure 2. MRI features of patients with MS who had antibodies to myelin oligodendrocyte glycoprotein (A) Patient 2: cerebral MRI showing typical MS deep white matter lesions (A.a, T2w, axial plane) and partially confluent callosal lesions (A.b, FLAIR, sagittal plane). Furthermore, bilateral lesions in the periaqueductal gray (A.c, T2w, A.d: magnified view) and bilateral pontomedullary lesions were observed (A.e, T2w, A.f: magnified view). sMRI displaying LETM and segmental atrophy in the lower thoracic and lumbar spinal cord (A.g, level T8-T11). (B) Patient 1: sMRI showing multiple partially confluent lesions in the cervical cord from C1-C6 (FLAIR, sagittal) and in the thoracic cord with focal atrophy. (C) Patient 3: sMRI demonstrating LETM from C2-C5 (FLAIR, sagittal). FLAIR = fluid-attenuated inversion recovery; LETM = longitudinally extensive transverse myelitis; MS = multiple sclerosis; sMRI = spinal MRI; T2w = T2-weighted.
Figure 2. MRI features of patients with MS who had antibodies to myelin oligodendrocyte glycoprotein (A) Patient 2: cerebral MRI showing typical MS deep white matter lesions (A.a, T2w, axial plane) and partially confluent callosal lesions (A.b, FLAIR, sagittal plane). Furthermore, bilateral lesions in the periaqueductal gray (A.c, T2w, A.d: magnified view) and bilateral pontomedullary lesions were observed (A.e, T2w, A.f: magnified view). sMRI displaying LETM and segmental atrophy in the lower thoracic and lumbar spinal cord (A.g, level T8-T11). (B) Patient 1: sMRI showing multiple partially confluent lesions in the cervical cord from C1-C6 (FLAIR, sagittal) and in the thoracic cord with focal atrophy. (C) Patient 3: sMRI demonstrating LETM from C2-C5 (FLAIR, sagittal). FLAIR = fluid-attenuated inversion recovery; LETM = longitudinally extensive transverse myelitis; MS = multiple sclerosis; sMRI = spinal MRI; T2w = T2-weighted.CC BY-NC-ND · PubMed Central

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Metadata

Authors
Spadaro, M., Gerdes, L. A., Krumbholz, M., Ertl-Wagner, B., Thaler, F. S., Schuh, E., Metz, I., Blaschek, A., Dick, A., Brück, W., Hohlfeld, R., Meinl, E., & Kümpfel, T.
Affiliations
Universitätsklinikum Tübingen (DE)
Corresponding author
Kümpfel, Tania
ORCID
Venue
Neurology Neuroimmunology & Neuroinflammation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2016-10
Volume
3
Issue
5
Pages
e257-e257
ISSN
2332-7812 (ISSN-L)
DOI
10.1212/nxi.0000000000000257
PMC
PMC4949775
OpenAlex
W2462819126
Cited by
206
References
38
Citations by year
2026: 2 · 2025: 7 · 2024: 9 · 2023: 8 · 2022: 11 · 2021: 18 · 2020: 34 · 2019: 41 · 2018: 35 · 2017: 37 · 2016: 2
FWCI
34.84
Type
journal article
Language
en
Open access
Licence
cc-by-nc-nd
Locations
  • Neurology Neuroimmunology & Neuroinflammation (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Open access LMU (Ludwid Maxmilian's Universitat Munchen) (submittedVersion)
Funders
  • Deutsche Forschungsgemeinschaft (TR‐128)
  • Gemeinnützige Hertie-Stiftung
  • Werner Reichenberger Stiftung
Topics
  • Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
  • Health Sciences › Medicine › Clinical Neurology › Autoimmune Neurological Disorders and Treatments
  • Health Sciences › Medicine › Clinical Neurology › Peripheral Neuropathies and Disorders
Keywords
myelin oligodendrocyte glycoprotein, anti-MOG antibodies, multiple sclerosis, disease heterogeneity, brainstem involvement, spinal cord involvement, optic nerve involvement, plasma exchange, epitope mapping, relapse

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