The interplay of IKK, NF‐κB and RIPK1 signaling in the regulation of cell death, tissue homeostasis and inflammation

Vangelis Kondylis; Snehlata Kumari; Katerina Vlantis; Manolis Pasparakis

doi:10.1111/imr.12550

journal article Apr 30, 2017

The interplay of IKK, NF‐κB and RIPK1 signaling in the regulation of cell death, tissue homeostasis and inflammation

Vangelis Kondylis

Snehlata Kumari

Katerina Vlantis Manolis Pasparakis

Immunological Reviews Vol. 277 No. 1 pp. 113-127 · Wiley

View at Publisher Save 10.1111/imr.12550

Abstract

SummaryRegulated cell death pathways have important functions in host defense and tissue homeostasis. Studies in genetic mouse models provided evidence that cell death could cause inflammation in different tissues. Inhibition of RIPK3‐MLKL‐dependent necroptosis by FADD and caspase‐8 was identified as a key mechanism preventing inflammation in epithelial barriers. Moreover, the interplay between IKK/NF‐κB and RIPK1 signaling was recognized as a critical determinant of tissue homeostasis and inflammation. NEMO was shown to regulate RIPK1 kinase activity‐mediated apoptosis by NF‐κB‐dependent and –independent functions, which are critical for averting chronic tissue injury and inflammation in the intestine and the liver. In addition, RIPK1 was shown to exhibit kinase activity‐independent functions that are essential for preventing cell death, maintaining tissue architecture and inhibiting inflammation. In the intestine, RIPK1 acts as a scaffold to prevent epithelial cell apoptosis and preserve tissue integrity. In the skin, RIPK1 functions via its RHIM to counteract ZBP1/DAI‐dependent activation of RIPK3‐MLKL‐dependent necroptosis and inflammation. Collectively, these studies provided evidence that the regulation of cell death signaling plays an important role in the maintenance of tissue homeostasis, and suggested that cell death could be causally involved in the pathogenesis of inflammatory diseases.

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Details

Published: Apr 30, 2017
Vol/Issue: 277(1)
Pages: 113-127
License: View

Authors

V

Vangelis Kondylis

Institute for Genetics University of Cologne Cologne Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging‐Associated Diseases (CECAD) University of Cologne Cologne Germany; Center for Molecular Medicine (CMMC) University of Cologne Cologne Germany

S

Snehlata Kumari

Institute for Genetics University of Cologne Cologne Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging‐Associated Diseases (CECAD) University of Cologne Cologne Germany; Center for Molecular Medicine (CMMC) University of Cologne Cologne Germany

K

Katerina Vlantis

Institute for Genetics University of Cologne Cologne Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging‐Associated Diseases (CECAD) University of Cologne Cologne Germany; Center for Molecular Medicine (CMMC) University of Cologne Cologne Germany

M

Manolis Pasparakis

Institute for Genetics University of Cologne Cologne Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging‐Associated Diseases (CECAD) University of Cologne Cologne Germany; Center for Molecular Medicine (CMMC) University of Cologne Cologne Germany

Funding

Deutsche Forschungsgemeinschaft Award: SFB670

European Commission Award: 223404

European Research Council Award: 323040

Worldwide Cancer Research Award: 15‐0228

Deutsche Krebshilfe Award: 110302

Cite This Article

Vangelis Kondylis, Snehlata Kumari, Katerina Vlantis, et al. (2017). The interplay of IKK, NF‐κB and RIPK1 signaling in the regulation of cell death, tissue homeostasis and inflammation. Immunological Reviews, 277(1), 113-127. https://doi.org/10.1111/imr.12550

The interplay of IKK, NF‐κB and RIPK1 signaling in the regulation of cell death, tissue homeostasis and inflammation

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