XIAP Loss Triggers RIPK3- and Caspase-8-Driven IL-1β Activation and Cell Death as a Consequence of TLR-MyD88-Induced cIAP1-TRAF2 Degradation

XIAP Loss Triggers RIPK3- and Caspase-8-Driven IL-1β Activation and Cell Death as a Consequence of TLR-MyD88-Induced cIAP1-TRAF2 Degradation

X-linked Inhibitor of Apoptosis (XIAP) deficiency predisposes people to pathogen-associated hyperinflammation. Upon XIAP loss, Toll-like receptor (TLR) ligation triggers RIPK3-caspase-8-mediated IL-1β activation and death in myeloid cells. How XIAP suppresses these events remains unclear. Here, we s...

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Bibliographic Details
Main Authors: Kate E. Lawlor, Rebecca Feltham, Monica Yabal, Stephanie A. Conos, Kaiwen W. Chen, Stephanie Ziehe, Carina Graß, Yifan Zhan, Tan A. Nguyen, Cathrine Hall, Angelina J. Vince, Simon M. Chatfield, Damian B. D’Silva, Kenneth C. Pang, Kate Schroder, John Silke, David L. Vaux, Philipp J. Jost, James E. Vince
Format: Article
Language:English
Published: Elsevier 2017-07-01
Series:Cell Reports
Subjects:
Toll-like receptor
NLRP3
RIPK3
caspase-8
TNFR2
XIAP
cIAP1
necroptosis
interferon
autoinflammatory disease
Online Access:http://www.sciencedirect.com/science/article/pii/S221112471730904X

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