Antibody-mediated remyelination operates through mechanism independent of immunomodulation

Bogoljub Ciric, Virginia Van Keulen, Mateo Paz Soldan, Moses Rodriguez, Larry R. Pease

Research output: Contribution to journalArticle

32 Scopus citations

Abstract

A set of antibodies capable of binding glial cells promotes remyelination in models of multiple sclerosis (MS). Within this set, the mouse antibody, SCH94.03, was immunomodulatory implying that immune system mobilization might be integral to remyelination. We evaluated whether the human remyelination-promoting antibody rHIgM22 influences acquired immunity. The antibody did not bind to immune cells, or influence humoral immune responses, antigen presentation, T cell proliferation or cytokine production. Treatment with rHIgM22 had no effect on demyelination or virus infection in two disease models. These results demonstrate that the remyelination-promoting activity of antibody rHIgM22 is not dependent on immunomodulation.

Original languageEnglish (US)
Pages (from-to)153-161
Number of pages9
JournalJournal of neuroimmunology
Volume146
Issue number1-2
DOIs
StatePublished - Jan 2004

Keywords

  • EAE
  • IgM
  • Immunomodulation
  • Multiple sclerosis
  • Remyelination

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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