Pristane induces autophagy in macrophages, promoting a STAT1-IRF1-TLR3 pathway and arthritis

Pristane induces autophagy in macrophages, promoting a STAT1-IRF1-TLR3 pathway and arthritis

Copyright © 2016 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 175(2017) vom: 15. Feb., Seite 56-68
1. Verfasser: Zhu, Wenhua (VerfasserIn)
Weitere Verfasser: Xu, Jing, Jiang, Congshan, Wang, Bo, Geng, Manman, Wu, Xiaoying, Hussain, Nazim, Gao, Ning, Han, Yan, Li, Dongmin, Lan, Xi, Ning, Qilan, Zhang, Fujun, Holmdahl, Rikard, Meng, Liesu, Lu, Shemin
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2017
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Autophagy Experimental arthritis Gene expression Macrophages TLR3 Interferon Regulatory Factor-1 Irf1 protein, rat STAT1 Transcription Factor mehr... Stat1 protein, rat TLR3 protein, rat Terpenes Toll-Like Receptor 3 pristane 26HZV48DT1
Beschreibung
Zusammenfassung:Copyright © 2016 Elsevier Inc. All rights reserved.
Autophagy is involved in both innate and adaptive immune regulation. We propose that autophagy regulates activation of TLR3 in macrophages and is thereby essential for development of pristane-induced arthritis. We found that pristane treatment induced autophagy in macrophages in vitro and in vivo, in spleen cells from pristane injected rats. The induced autophagy was associated with STAT1 phosphorylation and expression of IRF1 and TLR3. Blocking the pristane activated autophagy by Wortmannin and Bafilomycin A1 or by RNAi of Becn1 led to a downregulation of the associated STAT1-IRF1-TLR3 pathway. Most importantly, the development of arthritis was alleviated by suppressing either autophagy or TLR3. We conclude that pristane enhanced autophagy, leading to a STAT1-IRF1 controlled upregulation of TLR3 expression in macrophages, is a pathogenic mechanism in the development of arthritis
Beschreibung:Date Completed 05.06.2017
Date Revised 06.02.2018
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2016.11.017