Jueqi Chen, PhD

Assistant Professor of Microbiology
Committee on Microbiology
Research and Scholarly Interests: Biochemistry, Fluorescence Microscopy, Inflammation, Innate Immunity, Microbiology
Websites: Jueqi Chen Lab, Research Network Profile
Contact: jueqi@uchicago.edu
Graduate Programs: Microbiology, UChicago Biosciences, Committee on Immunology

Inflammasomes are multi-protein complexes that are responsible for the induction of proinflammatory cytokines and inflammatory cell death. They are unique in innate immune signaling because they can be triggered by a plethora of diverse signals from both pathogens and environmental danger. The research in our lab focuses on dissecting the molecular mechanisms of inflammasome pathways and studying how their dysfunction leads to defective host defense against various pathogenic microorganisms, as well as the impact on autoimmune diseases, neurodegeneration and metabolic syndromes.

Our lab utilizes diverse and complementary approaches, including biochemical assays, confocal fluorescence imaging, CRISPR knockout/rescue and animal models. Our recent study has uncovered the unexpected role of trans-Golgi network dispersion in inflammasome activation, and we are currently interested in studying how pathogens are able to evade or hijack these cellular signals to counter the host defense. We believe that these studies will unveil potential therapeutic targets for infectious diseases and many other human health problems.

UT Southwestern Medical Center
Dallas, TX
Postdoctoral Researcher - Immunology & Microbiology
2019

UT Southwestern Medical Center
Dallas, TX
Ph.D. - Biomedical Science
2014

Zhejiang University
Hangzhou, China
B.S. - Biotechnology
2009

PtdIns4P on dispersed trans-Golgi network mediates NLRP3 inflammasome activation.
PtdIns4P on dispersed trans-Golgi network mediates NLRP3 inflammasome activation. Nature. 2018 12; 564(7734):71-76.
PMID: 30487600

Detection of Microbial Infections Through Innate Immune Sensing of Nucleic Acids.
Detection of Microbial Infections Through Innate Immune Sensing of Nucleic Acids. Annu Rev Microbiol. 2018 Sep 08; 72:447-478.
PMID: 30200854

Prion-like polymerization underlies signal transduction in antiviral immune defense and inflammasome activation.
Prion-like polymerization underlies signal transduction in antiviral immune defense and inflammasome activation. Cell. 2014 Mar 13; 156(6):1207-1222.
PMID: 24630723

MAVS recruits multiple ubiquitin E3 ligases to activate antiviral signaling cascades.
MAVS recruits multiple ubiquitin E3 ligases to activate antiviral signaling cascades. Elife. 2013 Aug 14; 2:e00785.
PMID: 23951545

Regulation of NF-?B by ubiquitination.
Regulation of NF-?B by ubiquitination. Curr Opin Immunol. 2013 Feb; 25(1):4-12.
PMID: 23312890

Direct, noncatalytic mechanism of IKK inhibition by A20.
Direct, noncatalytic mechanism of IKK inhibition by A20. Mol Cell. 2011 Nov 18; 44(4):559-71.
PMID: 22099304

Production of TH1 and TH2 cell lines and clones.
Fitch FW, Gajewski TF, Hu-Li J. Production of TH1 and TH2 cell lines and clones. Curr Protoc Immunol. 2006 May; Chapter 3:Unit 3.13.
PMID: 30487600