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

Author

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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)

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.

Suggested Citation

  • Patrick-Simon Welz & Andy Wullaert & Katerina Vlantis & Vangelis Kondylis & Vanesa Fernández-Majada & Maria Ermolaeva & Petra Kirsch & Anja Sterner-Kock & Geert van Loo & Manolis Pasparakis, 2011. "FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation," Nature, Nature, vol. 477(7364), pages 330-334, September.
    • Handle: RePEc:nat:nature:v:477:y:2011:i:7364:d:10.1038_nature10273
    DOI: 10.1038/nature10273
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    Cited by:

    1. Chunxiao Liu & Hui Wang & Lu Han & Yifan Zhu & Shurui Ni & Jingke Zhi & Xiping Yang & Jiayi Zhi & Tian Sheng & Huanqiu Li & Qinghua Hu, 2024. "Targeting P2Y14R protects against necroptosis of intestinal epithelial cells through PKA/CREB/RIPK1 axis in ulcerative colitis," Nature Communications, Nature, vol. 15(1), pages 1-16, December.

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