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

Authors

Chandirasegara Massilamany, University of Nebraska-LincolnFollow
Arunakumar Gangaplara, University of Nebraska-Lincoln
Heejeong Kim, University of Nebraska-LincolnFollow
Charlotte Standord, University of Nebraska-Lincoln
Govardhan Rathnaiah, University of Nebraska-LincolnFollow
David Steffen, University of Nebraska-LincolnFollow
Jaekwon Lee, University of Nebraska-LincolnFollow
Jay Reddy, University of Nebraska-LincolnFollow

Document Type

Article

Date of this Version

2012

Citation

J Neuroimmunol. 2013 March 15; 256(0): 19–27. doi:10.1016/j.jneuroim.2012.12.004

Comments

Copyright 2012. Used by permission.

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.