Mice lacking myeloperoxidase are more susceptible to experimental autoimmune encephalomyelitis

J Neuroimmunol. 2001 Jan 1;112(1-2):97-105. doi: 10.1016/s0165-5728(00)00392-1.


EAE is a demyelinating disease which serves as an animal model for multiple sclerosis (MS). Myeloperoxidase (MPO) has been implicated in MS through its presence in invading macrophages, and by association of a -463G/A promoter polymorphism with increased risk. Also, MPO at 17q23.1 is within a region identified in genome scans as a MS susceptibility locus. We here examine the incidence of EAE in MPO knockout (KO) mice. MPO is detected in invading macrophages in the CNS of wild-type mice, yet unexpectedly, MPO-KO mice have significantly increased incidence of EAE: Ninety percent of MPO-KO mice developed complete hind limb paralysis as compared to 33% of wildtype (WT) littermates (P<0.0001). This is the first evidence that MPO plays a significant role in EAE, consistent with its postulated role in MS.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Disease Susceptibility
  • Encephalomyelitis, Autoimmune, Experimental / etiology*
  • Interferon-gamma / physiology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nitric Oxide Synthase / physiology
  • Nitric Oxide Synthase Type II
  • Peroxidase / deficiency
  • Peroxidase / physiology*


  • Interferon-gamma
  • Peroxidase
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse