Myelin oligodendrocyte glycoprotein antibodies in pathologically proven multiple sclerosis: frequency, stability and clinicopathologic correlations

• Published in: Multiple sclerosis 2007-01, Vol.13 (1), p.7-16
• Main Authors: Pittock, S J, Reindl, M, Achenbach, S, Berger, T, Bruck, W, Konig, F, Morales, Y, Lassmann, H, Bryant, S, Moore, S B, Keegan, B M, Lucchinetti, C F
• Format: Article
• Language: English
• Subjects: Autoantibodies - blood; Biological and medical sciences; Biomarkers - blood; Blotting, Western; Cohort Studies; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Demyelinating Diseases - genetics; Demyelinating Diseases - immunology; Demyelinating Diseases - pathology; Enzyme-Linked Immunosorbent Assay; Genotype; HLA-DR2 Antigen - genetics; Humans; Immunomodulators; Medical sciences; Multiple Sclerosis - genetics; Multiple Sclerosis - immunology; Multiple Sclerosis - pathology; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis; Myelin Proteins; Myelin-Associated Glycoprotein - immunology; Myelin-Oligodendrocyte Glycoprotein; Neurology; Pharmacology. Drug treatments; Plasmapheresis; Predictive Value of Tests
• ISSN: 1352-4585; 1477-0970
• DOI: 10.1177/1352458506072189

Controversy exists regarding the pathogenic or predictive role of anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with multiple sclerosis (MS). Four immunopathological patterns (IP) have been recognized in early active MS lesions, suggesting heterogeneous pathogenic mechanisms. Whether MOG antibodies contribute to this pathological heterogeneity and potentially serve as biomarkers to identify specific pathological patterns is unknown. Here we report the frequencies of antibodies to human recombinant MOG (identified by Western blot and enzymelinked immunoabsorbent assay (ELISA)) in patients with pathologically proven demyelinating disease, and investigate whether antibody status is associated with clinical course, HLA-DR2 genotype, IP or treatment response to plasmapheresis. The biopsy cohort consisted of 72 patients: 12 pattern I, 43 pattern II and 17 pattern III. No association was found between MOG antibody status and conversion to clinically definite MS, DR-2 status, IP or response to plasmapheresis. There was poor agreement between Western blot and ELISA (kappa=0.07 for MOG IgM). Fluctuations in antibody seropositivity were seen for 3/4 patients tested serially by Western blot. This study does not support a pathologic pattern-specific role for MOG-antibodies. Variable MOG-antibody status on serial measurements, coupled with the lack of Western blot and ELISA correlations, raises concern regarding the use of MOG-antibody as an MS biomarker and underscores the need for methodological consensus.