Name:Rongbin Zhou(周荣斌)
Address:School of Life Sciences, University of Science and Technology of

China, 230026 Hefei, P. R. China
09/1998-06/2002B.S., University of Science & Technology of China
09/2002-06/2007Ph.D, University of Science & Technology of China
07/2007-02/2011Postdoc, University of Lausanne, Switzerland
03/2011-presentProfessor, University of Science & Technology of China
Our general interest is to understand how pathogen and danger signal trigger innate immunity and inflammation, and includes the following areas:
1.Molecular mechanisms of innate immune recognition and signal transduction: 
Analysis of the receptors (pattern recognition receptors, PRRs) the involved in innate immune recognition, including identification of new activators and clarification of the signaling transduction pathways. Our particular interest is to understand the signaling networks that control the activation of “inflmmaosme”.
2.Basic biology of inflammation:
Inflammation is a fundamental biological response to harmful stimuli, such as pathogens and danger. We are studying the signaling networks that control the initiation, progression and termination of inflammatory responses. We also have interest to understand the links between inflammation and metabolism disorder, inflammation and cancer.
1.Huang Y, Jiang H, Chen Y, Wang X, Yang Y, Tao J, Deng X, Liang G, Zhang H, Jiang W, Zhou R. Tranilast directly targets NLRP3 to treat inflammasome-driven  diseases. EMBO Mol Med. 2018 Apr;10(4). pii: e8689. doi: 10.15252/emmm.201708689.
2.Gong T, Yang Y, Jin T, Jiang W, Zhou R. Orchestration of NLRP3 Inflammasome Activation by Ion Fluxes. Trends Immunol. 2018 May;39(5):393-406.
3.Jiang H, He H, Chen Y, Huang W, Cheng J, Ye J, Wang A, Tao J, Wang C, Liu Q, Jin T, Jiang W, Deng X, Zhou R. Identification of a selective and direct NLRP3 inhibitor to treat inflammatory disorders. J Exp Med. 2017 Nov 6;214(11):3219-3238
4.Tang T, Lang X, Xu C, Wang X, Gong T, Yang Y, Cui J, Bai L, Wang J, Jiang W, Zhou R. CLICs-dependent chloride efflux is an essential and proximal upstream event for NLRP3 inflammasome activation. Nat Commun. 2017 Aug 4;8(1):202
5.Yan Y, Jiang W, Liu L, Wang X, Ding C, Tian Z, Zhou R. Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome. Cell. 2015 Jan 15;160(1-2):62-73.
6.Wang X, Jiang W, Yan Y, Gong T, Han J, Tian Z, Zhou R. RNA viruses promote activation of the NLRP3 inflammasome through a RIP1-RIP3-DRP1 signaling pathway. Nat Immunol. 2014 ;15(12):1126-33.
7.Lang X, Tang T, Jin T, Ding C, Zhou R, Jiang W. TRIM65-catalized ubiquitination is essential for MDA5-mediated antiviral innate immunity. J Exp Med. 2017 Feb;214(2):459-473
8.Jiang W, Wang X, Zeng B, Liu L, Tardivel A, Wei H, Han J, MacDonald HR, Tschopp J, Tian Z, Zhou R. Recognition of gut microbiota by NOD2 is essential for the homeostasis of intestinal intraepithelial lymphocytes. J Exp Med. 2013;21;210(11):2465-76.
9.Yan Y, Jiang W, Spinetti T, Tardivel A, Castillo R, Bourquin C, Guarda G, Tian Z, Tschopp J, Zhou R. ω-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation. Immunity. 2013 Jun 27;38(6):1154-63.
10.Zhou R, Yazdi A, Menu P,Tschopp J. A role for mitochondria in NLRP3 inflammasome activation. Nature. 2011 Jan 13;469(7329):221-5
11.Zhou R, Tardivel A, Thorens B, Choi I, Tschopp J. Thioredoxin-interacting protein links oxidative stress to inflammasome activation. Nat Immunol. 2010 Feb;11(2):136-40.
12.Schroder K, Zhou R, Tschopp J. The NLRP3 inflammasome: a sensor for metabolic danger? Science. 2010 Jan 15;327(5963):296-300.

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