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Suppression of the TRIF-dependent signaling pathway of toll-like receptor by triptolide

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Suppression of the TRIF-dependent signaling pathway of toll-like receptor by triptolide

Content Provider	Springer Nature Link
Author	Gu, Gyo Jeong Youn, Hyung Sun
Copyright Year	2013
Abstract	Toll-like receptors (TLRs) recognize specific patterns derived from invading microbial pathogens. TLR activation by microbial components triggers the activation of myeloid differential factor 88 (MyD88)- and tollinterleukin-1 receptor domain-containing adapter inducing interferon-β (TRIF)-dependent downstream signaling pathways, leading to the activation of nuclear factor-κB (NF-κB) and interferon regulatory factor 3 (IRF3). Triptolide (TP), an active ingredient of Tripterygium wilfordii Hook. F, has been reported to have positive effects on autoimmune and inflammatory diseases. To evaluate the therapeutic potential of TP, its effect on signal transduction via the TRIF-dependent pathway of TLRs induced by lipopolysaccharide (LPS) or polyinosinic-polycytidylic acid (poly[I:C]) was examined. TP inhibited NF-κB and IRF3 activation and IRF3 phosphorylation induced by LPS or poly[I:C]. TP also inhibited interferon-inducible genes such as, interferon inducible protein-10. These results suggest that TP can modulate TRIF-dependent signaling pathways of TLRs, and will become promising drug candidates in TLRs-based therapy in the future.
Starting Page	177
Ending Page	182
Page Count	6
File Format	PDF
ISSN	20059752
Journal	Toxicology and Environmental Health Sciences
Volume Number	5
Issue Number	4
e-ISSN	22337784
Language	English
Publisher	Springer Netherlands
Publisher Date	2014-02-02
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Toll-like receptors triptolide lipopolysaccharide polyinosinic-polycytidylic acid TRIF Pharmacology/Toxicology Environmental Health
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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