FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation

Patrick-Simon Welz, Andy Wullaert, Katerina Vlantis, Vangelis Kondylis, Vanesa Fernández-Majada, Maria Ermolaeva, Petra Kirsch, Anja Sterner-Kock, Geert van Loo and Manolis Pasparakis ()
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Patrick-Simon Welz: Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Str. 47a
Andy Wullaert: Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Str. 47a
Katerina Vlantis: Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Str. 47a
Vangelis Kondylis: Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Str. 47a
Vanesa Fernández-Majada: Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Str. 47a
Maria Ermolaeva: Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Str. 47a
Petra Kirsch: Tierforschungszentrum, University of Ulm, Albert-Einstein-Allee 11
Anja Sterner-Kock: Center for Experimental Medicine, Uniklinik Köln, University of Cologne, Robert- Kochstr. 10
Geert van Loo: VIB, Ghent University, Technologiepark 927
Manolis Pasparakis: Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Str. 47a

Nature, 2011, vol. 477, issue 7364, 330-334

Abstract: Epithelial cell death in intestinal inflammatory disease Two groups identify the regulation of death-receptor-induced necroptosis as an epithelial intrinsic mechanism that is important for the maintenance of immune homeostasis and the prevention of intestinal inflammation in mice. Welz et al. describe an unexpected physiological function for FADD (Fas-associated protein with death domain), an adaptor protein required for death-receptor-induced apoptosis. Mice with intestinal epithelial specific knockout of FADD develop severe colon inflammation due to increased death of FADD-deficient colonic epithelial cells. Günther et al. report a novel and unexpected function of caspase-8 in maintaining immune homeostasis in the gut. Caspase-8 expression by gut epithelial cells is shown to protect mice from TNF-mediated Paneth cell death and intestinal inflammation. Increased expression of the protein RIP3 was associated with the TNF-induced pathology, and elevated RIP3 expression was also found in intestinal Paneth cells of patients with Crohn's disease.

Date: 2011
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DOI: 10.1038/nature10273

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