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Molecular Mechanisms of Oligodendrocyte Injury in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis
Multiple Sclerosis Center, Department of Neurological Sciences, Rush University Medical Center, 1725 W. Harrison, Suite 309, Chicago, IL 60612, USA
* Author to whom correspondence should be addressed.
Received: 16 July 2012; in revised form: 20 August 2012 / Accepted: 20 August 2012 / Published: 23 August 2012
Abstract: New evidence has emerged over the last decade indicating that oligodendrocyte injury in multiple sclerosis (MS) is not a single unified phenomenon but rather a spectrum of processes ranging from massive immune destruction to a subtle cell death in the absence of significant inflammation. Experimentally, protection of oligodendrocytes against inflammatory injury results in protection against experimental autoimmune encephalitis, the animal model of multiple sclerosis. In this review, we will discuss the molecular mechanisms regulating oligodendrocyte injury and inflammatory demyelination. We draw attention to the injurious role of IFN-γ signaling in oligodendrocytes and the pro-inflammatory effect of their death. In conclusion, studying the molecular mechanisms of oligodendrocyte injury is likely to provide new perspective on the pathogenesis of MS and a rationale for cell protective therapies.
Keywords: multiple sclerosis; pathology; oligodendrocytes; cell signaling; interferon regulatory factor 1; Caspase 1
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Patel, J.; Balabanov, R. Molecular Mechanisms of Oligodendrocyte Injury in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis. Int. J. Mol. Sci. 2012, 13, 10647-10659.
Patel J, Balabanov R. Molecular Mechanisms of Oligodendrocyte Injury in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis. International Journal of Molecular Sciences. 2012; 13(8):10647-10659.
Patel, Jilpa; Balabanov, Roumen. 2012. "Molecular Mechanisms of Oligodendrocyte Injury in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis." Int. J. Mol. Sci. 13, no. 8: 10647-10659.