| First Author | Massilamany C | Year | 2013 |
| Journal | J Neuroimmunol | Volume | 256 |
| Issue | 1-2 | Pages | 19-27 |
| PubMed ID | 23294897 | Mgi Jnum | J:309955 |
| Mgi Id | MGI:6760088 | Doi | 10.1016/j.jneuroim.2012.12.004 |
| Citation | Massilamany C, et al. (2013) Copper-zinc superoxide dismutase-deficient mice show increased susceptibility to experimental autoimmune encephalomyelitis induced with myelin oligodendrocyte glycoprotein 35-55. J Neuroimmunol 256(1-2):19-27 |
| abstractText | 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. |
