Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6020456 | Journal of Neuroimmunology | 2013 | 9 Pages |
Abstract
Autoimmune diseases such as multiple sclerosis (MS) are thought to develop due to a dysregulation in the normal TH1-TH17/TH2 immune system balance, where pro-inflammatory responses with a TH1/TH17 prevalence develop. Some therapeutic treatments in MS promote a shift toward a TH2-prevalent environment and this has been shown to be protective. However, not all patients respond to current immunomodulatory treatments in MS so that new immunomodulatory drugs that can promote a shift of the immune system into an anti-inflammatory TH2 status are needed. IL-25 is a cytokine of the IL-17 family with powerful anti-inflammatory properties. This study demonstrates that IL-25 exerts neuroprotective functions by reducing T cell-mediated killing of human fetal neurons. The mechanism of action of this IL-25-mediated neuroprotective effect appears to be linked to reduction in the expression of the adhesion molecule LFA-1, which is relevant in stabilizing the immune synapse during cytotoxicity.
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Authors
Diane A. Turner, Yohannes Haile, Fabrizio Giuliani,