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Neurology. 2011 Aug 9;77(6):580-8. doi: 10.1212/WNL.0b013e318228c0b1. Epub 2011 Jul 27.

Antibodies to MOG are transient in childhood acute disseminated encephalomyelitis.

Author information

1
Max Planck Institute of Neurobiology, Department of Neuroimmunology, Martinsried, Germany.

Abstract

OBJECTIVE:

To study the longitudinal dynamics of anti-myelin oligodendrocyte glycoprotein (MOG) autoantibodies in childhood demyelinating diseases.

METHODS:

We addressed the kinetics of anti-MOG immunoglobulins in a prospective study comprising 77 pediatric patients. This was supplemented by a cross-sectional study analyzing 126 pediatric patients with acute demyelination and 62 adult patients with multiple sclerosis (MS). MOG-transfected cells were used for detection of antibodies by flow cytometry.

RESULTS:

Twenty-five children who were anti-MOG immunoglobulin (Ig) positive at disease onset were followed for up to 5 years. Anti-MOG antibodies rapidly and continuously declined in all 16 monophasic patients with acute disseminated encephalomyelitis and in one patient with clinically isolated syndrome. 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. Antibodies to MOG were mainly IgG 1 and their binding was largely blocked by pathogenic anti-MOG antibodies derived from a spontaneous animal model of autoimmune encephalitis. The cross-sectional part of our study elaborated that anti-MOG Ig was present in about 25% of children with acute demyelination, but in none of the pediatric or adult controls. Sera from 4/62 (6%) adult patients with MS had anti-MOG IgG at low levels.

CONCLUSIONS:

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

PMID:
21795651
DOI:
10.1212/WNL.0b013e318228c0b1
[Indexed for MEDLINE]

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