Copper-zinc superoxide dismutase-deficient mice show increased susceptibility to experimental autoimmune encephalomyelitis induced with myelin oligodendrocyte glycoprotein 35-55

Chandirasegaran Massilamany, Arunakumar Gangaplara, Heejeong Kim, Charlotte Stanford, Govardhan Rathnaiah, David Steffen, Jaekwon Lee, Jay Reddy

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

In this report, we have addressed the role of copper-zinc superoxide dismutase (SOD1) deficiency in the mediation of central nervous system autoimmunity. We demonstrate that SOD1-deficient C57Bl/6 mice develop more severe autoimmune encephalomyelitis induced with myelin oligodendrocyte glycoprotein (MOG) 35-55, compared with wild type mice. This alteration in the disease phenotype was not due to aberrant expansion of MOG-specific T cells nor their ability to produce inflammatory cytokines; rather lymphocytes generated in SOD1-deficient mice were more prone to spontaneous cell death when compared with their wild type littermate controls. The data point to a role for SOD1 in the maintenance of self-tolerance leading to the suppression of autoimmune responses.

Original languageEnglish (US)
Pages (from-to)19-27
Number of pages9
JournalJournal of Neuroimmunology
Volume256
Issue number1-2
DOIs
StatePublished - Mar 15 2013

Keywords

  • Autoimmunity
  • Experimental autoimmune encephalomyelitis
  • Oxidative stress
  • T cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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