Do antibodies stimulate myelin repair in multiple sclerosis?

Dorian Mcgavern, Kunihiko Asakura, Moses Rodriquez

Research output: Contribution to journalReview articlepeer-review

11 Scopus citations


One of the major goals in the study of multiple sclerosis (MS) is to identify a beneficial therapeutic intervention that mimics the intrinsic reparative process and results in longterm clinical improvement. As yet, the therapeutic strategies tested in MS have failed to accomplish this task. However, one potential therapy that has shown some promise in rodent models of demyelination involves the administration of antibodies. Studies in various models of demyelination (virus-induced, autoimmune, and toxic) indicate that a subset of autoantibodies with reactivity to CNS antigens promote remyelination. We have identified a prototypic germline IgMk monoclonal antibody, designated SCH 94.03, with reactivity to a surface antigen on oligodendrocytes that promotes CNS remyelination. This antibody has the phenotypic features of polyreactive physiological natural autoantibodies. Additionally, treatment of MS patients with intravenous immunoglobulin, which contains these natural autoantibodies, may be efficacious in a subset of patients. We propose three mechanisms (direct stimulation of oligodendrocytes, immunomodulation, and opsonization of debris) by which polyreactive natural autoantibodies directed against CNS antigen may promote remyelination. Remyelination has the potential to not only improve conduction velocity but also may protect axons from injury and improve neurological function.

Original languageEnglish (US)
Pages (from-to)19-28
Number of pages10
Issue number1
StatePublished - Jan 1999


  • Autoantibodies
  • Oligodendrocytes
  • Remyelination
  • Theiler's virus

ASJC Scopus subject areas

  • General Neuroscience
  • Clinical Neurology


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