Therapeutic depletion of monocyte-derived cells protects from long-term axonal loss in experimental autoimmune encephalomyelitis

Monica A. Moreno, Travis Burns, Pamela Yao, Laird Miers, David E Pleasure, Athena Soulika

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

Studies in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE) suggest that peripheral monocyte-derived cells (MDCs) are instrumental for disease initiation. MDCs, however, are plastic, and may exert various functions once in the central nervous system (CNS) for prolonged periods. Furthermore, the long-term effect of MDC depletion on continuing axon loss is not known. We show that long-lasting depletion of MDCs, after onset of EAE clinical deficits, is accompanied by decreased CNS infiltration by pathogenic T lymphocytes. Although this treatment does not reverse clinical disease, it prevents worsening of neurological deficits and long-term axonal loss.

Original languageEnglish (US)
Pages (from-to)36-46
Number of pages11
JournalJournal of Neuroimmunology
Volume290
DOIs
StatePublished - Jan 15 2016

Keywords

  • Axonal protection
  • Clodronate
  • EAE
  • Macrophages
  • Microglia
  • Monocyte-derived cells

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

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