Accelerated axon loss in MOG35-55 experimental autoimmune encephalomyelitis (EAE) in myelin-associated glycoprotein-deficient (MAGKO) mice

Melina V. Jones, Thien T. Nguyen, Osefame Ewaleifoh, Lori Lebson, Katherine A. Whartenby, John W. Griffin, Peter A. Calabresi

Research output: Contribution to journalArticlepeer-review

Abstract

Myelin-associated glycoprotein (MAG) expressed by oligodendrocytes promotes the stability of axons but also impedes neural repair by inhibiting axon extension through lesioned white matter. We previously reported exacerbated axon losses in MAGKO as compared to wild type mice, 30. days into experimental autoimmune encephalitis (EAE). Here, we report the time course of axon losses in EAE and show this occurs as early as 7. days post-immunization, confirming MAG is protective against immune-mediated axon transection events. MAGKO mice also exhibit increased microglial activation prior to EAE, which is not seen in B4galnt1KO mice that also have axon loss, suggesting that the microglial activation may be a consequence of the loss of MAG inhibitory influence, and not a simple result of axonal degeneration.

Original languageEnglish (US)
Pages (from-to)53-61
Number of pages9
JournalJournal of Neuroimmunology
Volume262
Issue number1-2
DOIs
StatePublished - 2013

Keywords

  • B4galnt1KO
  • EAE
  • MAG
  • Microglia
  • T cell
  • Timeline

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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