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Sci. Signal., 22 May 2012
Vol. 5, Issue 225, p. ra38
[DOI: 10.1126/scisignal.2002767]


Editor's Summary

Inflammasome Dependency Determines Therapy?
Multiple sclerosis (MS) is an inflammatory autoimmune disease in which the myelin sheath surrounding axons is destroyed by cells of the immune system. MS and experimental autoimmune encephalitis (EAE), an animal model of MS, can be ameliorated by interferon-β (IFN-β); however, IFN-β is not effective in all cases. Inoue et al. determined a mechanism by which IFN-β decreases the severity of EAE in mice by inhibiting the activity of the NLRP3 inflammasome. However, the authors also characterized a form of EAE that was independent of NLRP3 and was refractory to IFN-β. Given other reports that have suggested the involvement of inflammasomes in MS, it will be important to investigate whether patients who fail to respond to IFN-β have inflammasome-independent disease.

Citation: M. Inoue, K. L. Williams, T. Oliver, P. Vandenabeele, J. V. Rajan, E. A. Miao, M. L. Shinohara, Interferon-β Therapy Against EAE Is Effective Only When Development of the Disease Depends on the NLRP3 Inflammasome. Sci. Signal. 5, ra38 (2012).

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