کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6020456 | 1580409 | 2013 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IL-25 prevents T cell-mediated neurotoxicity by decreasing LFA-1 expression
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
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چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Neuroimmunology - Volume 265, Issues 1â2, 15 December 2013, Pages 11-19
Journal: Journal of Neuroimmunology - Volume 265, Issues 1â2, 15 December 2013, Pages 11-19
نویسندگان
Diane A. Turner, Yohannes Haile, Fabrizio Giuliani,