The Absence of the Pro-Antioxidant Transcription Factor Nrf2 Exacerbates Experimental Autoimmune Encephalomyelitis

Summary: Disruption of Nrf2 resulted in a more severe clinical course, a more rapid onset, and a greater percentage of mice with the disease. Furthermore, increased immune cell infiltration and glial cell activation in spine was observed. In conjunction, we observed increased inflammatory enzyme (iNOS, phox-47, gp91-phox and phox-67), cytokine (IFN-gamma, IL1-b, TNF-alpha, and IL-12) and chemokine (BLC, MIG) gene expression levels in the Nrf2 deficient mice compared to the WT mice, supporting the notion that Nrf2 can modulate an autoimmune neuroinflammatory response. Our results show that the absence of Nrf2 exacerbates the development of EAE and thus suggests that activation of Nrf2 may then attenuate pathogenesis of autoimmune diseases such as multiple sclerosis as well as neurodegenerative diseases.


Johnson, D. A., Amirahmadi, S., Ward, C., Fabry, Z., and Johnson, J. A. (2009). The absence of the pro-antioxidant transcription factor nrf2 exacerbates experimental autoimmune encephalomyelitis. Toxicol. Sci., pages kfp274+. http://www.citeulike.org/user/HEIRS/article/6208104