Abstract
The article by Johnson et al. on the role of antioxidant signaling pathways in a model of experimental autoimmune encephalomyelitis (EAE) merits further discussion. This group hypothesized that alterations in oxidative signaling may be involved in the development of EAE and multiple sclerosis (MS). Their laboratory has performed extensive characterization of the nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) pathway and the Nrf2 knockout mice. Building upon their previous studies, they have extended their characterization of the Nrf2-ARE system in an autoimmune inflammatory model of MS by crossing the Biozzi ABH mice with Nrf2 knockout mice. These hybrid mice allowed a direct test of their hypothesis and were crucial for the success of these studies. In this study, the authors demonstrate that the loss of Nrf2 exacerbates the development of EAE, suggesting that Nrf2 may represent a common pathway and that activation of Nrf2 may attenuate pathogenesis of autoimmune and neurodegenerative diseases.
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