CLICs-dependent chloride efflux is an essential and proximal upstream event for NLRP3 inflammasome activation

Tiantian Tang; Xueting Lang; Congfei Xu; Xiaqiong Wang; Tao Gong; Yanqing Yang; Jun Cui; Li Bai; Jun Wang; Wei Jiang; Rongbin Zhou

doi:10.1038/s41467-017-00227-x

Nature Communications (Aug 2017)

CLICs-dependent chloride efflux is an essential and proximal upstream event for NLRP3 inflammasome activation

Tiantian Tang,
Xueting Lang,
Congfei Xu,
Xiaqiong Wang,
Tao Gong,
Yanqing Yang,
Jun Cui,
Li Bai,
Jun Wang,
Wei Jiang,
Rongbin Zhou

Affiliations

Tiantian Tang: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China
Xueting Lang: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China
Congfei Xu: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China
Xiaqiong Wang: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China
Tao Gong: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China
Yanqing Yang: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China
Jun Cui: Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University
Li Bai: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China
Jun Wang: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China
Wei Jiang: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China
Rongbin Zhou: Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China

DOI: https://doi.org/10.1038/s41467-017-00227-x
Journal volume & issue: Vol. 8, no. 1
pp. 1 – 12

Abstract

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The NLRP3 inflammasome is key to the regulation of innate immunity against pathogens or stress, but the underlying signaling regulation is still unclear. Here the authors show that chloride intracellular channels (CLIC) interface between mitochondria stress and inflammasome activation to modulate inflammatory responses.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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