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Publication : Mice lacking myeloperoxidase are more susceptible to experimental autoimmune encephalomyelitis.

First Author  Brennan M Year  2001
Journal  J Neuroimmunol Volume  112
Issue  1-2 Pages  97-105
PubMed ID  11108938 Mgi Jnum  J:102965
Mgi Id  MGI:3608278 Doi  10.1016/s0165-5728(00)00392-1
Citation  Brennan M, et al. (2001) Mice lacking myeloperoxidase are more susceptible to experimental autoimmune encephalomyelitis. J Neuroimmunol 112(1-2):97-105
abstractText  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.
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