4.7 Article

Antibodies to MOG are transient in childhood acute disseminated encephalomyelitis

期刊

NEUROLOGY
卷 77, 期 6, 页码 580-588

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e318228c0b1

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资金

  1. Deutsche Forschungsgemeinschaft [Sonderforschungsbereich 571]
  2. BMBF (Krankheitsbezogenes Kompetenznetz Multiple Sklerose), Excellence Initiative of the Ludwig-Maximilians-University Munich
  3. FoeFoLe of the Ludwig-Maximilians-University
  4. Gemeinnutzige Hertie Stiftung
  5. Research Foundation of the MS Society of Canada to the Canadian Pediatric Demyelinating Disease Study Group
  6. Bayer Schering Pharma
  7. Teva Pharmaceutical Industries Ltd.
  8. Merck Serono
  9. Novartis
  10. Biogen Idec
  11. BMBF
  12. ENS
  13. University of Wisconsin
  14. CMSC
  15. LACTRIMS
  16. NMSS
  17. sanofi-aventis
  18. Swedish Research Council
  19. EU
  20. Soderbergs Foundation
  21. Bibbi and Nils Jensens Foundation
  22. Montel Williams Foundation
  23. Swedish Brain foundation
  24. Tourette Syndrome Association, USA
  25. Brain Foundation Australia
  26. Trish Multiple Sclerosis Foundation Australia
  27. American Tourette Syndrome Association
  28. Brain Foundation
  29. Multiple Sclerosis Society of Canada
  30. Multiple Sclerosis Scientific Research Foundation
  31. Canadian Institutes of Health Research
  32. Genentech, Inc.
  33. Novartis Foundation
  34. German Research Foundation
  35. Swiss MS Society

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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. Neurology (R) 2011;77:580-588

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