کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5530736 | 1549389 | 2016 | 6 صفحه PDF | دانلود رایگان |
- Extracellular poly(I:C) activates TLR3-dependent IFN-β expression in HCT116.
- MAVS silencing upregulates IFN-β production via upregulation of NF-κB and IRF3 signaling.
- TLR3 signaling is regulated by miniMAVS, a 50Â kDa isoform of MAVS.
Innate immune responses to dsRNA result in signaling through the TLR3 pathway and/or the RIG-I/MDA-5/MAVS pathway which can activate type I IFN, proinflammatory cytokines and apoptosis. It is not clear whether MAVS could play a role in TLR3-dependent responses to extracellular dsRNA. Using a model of epithelial cells that express a functional TLR3 signaling pathway, we found that TLR3-dependent responses to extracellular dsRNA are negatively regulated by MAVS, precisely “miniMAVS”, a recently described 50Â kDa isoform of MAVS. This regulation of TLR3 by a MAVS isoform constitutes an endogenous regulatory mechanism in epithelial cells that could help prevent a potentially damaging excessive inflammatory response.
Journal: Cellular Immunology - Volume 310, December 2016, Pages 205-210