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

Department of Neurology, Mayo Clinic, Rochester, MN, USA

M Reindl

Clinical Department of Neurology, Innsbruck Medical University, Innsbruck, Austria

S Achenbach

Department of Biostatistics, Mayo Clinic, Rochester, MN, USA

T Berger

Clinical Department of Neurology, Innsbruck Medical University, Innsbruck, Austria

W Bruck

F Konig

Department of Neuropathology, University of Göttingen, Goöttingen, Germany

Y Morales

Department of Neurology, Mayo Clinic, Rochester, MN, USA

H Lassmann

Brain Research Institute, University of Vienna, Vienna, Austria

S Bryant

Department of Biostatistics, Mayo Clinic, Rochester, MN, USA

S B Moore

Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA

B M Keegan

Department of Neurology, Mayo Clinic, Rochester, MN, USA

C F Lucchinetti

Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN, USA. lucchinetti.claudia{at}mayo.edu

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.

Key Words: ELISA • immunological patterns • MOG antibodies • multiple sclerosis • Western blot

Multiple Sclerosis, Vol. 13, No. 1, 7-16 (2007)
DOI: 10.1177/1352458506072189


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