Antibodies to MOG are transient in childhood acute disseminated encephalomyelitis.

نویسندگان

  • A K Pröbstel
  • K Dornmair
  • R Bittner
  • P Sperl
  • D Jenne
  • S Magalhaes
  • A Villalobos
  • C Breithaupt
  • R Weissert
  • U Jacob
  • M Krumbholz
  • T Kuempfel
  • A Blaschek
  • W Stark
  • J Gärtner
  • D Pohl
  • K Rostasy
  • F Weber
  • I Forne
  • M Khademi
  • T Olsson
  • F Brilot
  • E Tantsis
  • R C Dale
  • H Wekerle
  • R Hohlfeld
  • B Banwell
  • A Bar-Or
  • E Meinl
  • T Derfuss
چکیده

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.

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عنوان ژورنال:
  • Neurology

دوره 77 6  شماره 

صفحات  -

تاریخ انتشار 2011