Caspase-8 regulates TNF-α-induced epithelial necroptosis and terminal ileitis

Claudia Günther, Eva Martini, Nadine Wittkopf, Kerstin Amann, Benno Weigmann, Helmut Neumann, Maximilian J. Waldner, Stephen M. Hedrick, Stefan Tenzer, Markus F. Neurath and Christoph Becker ()
Additional contact information
Claudia Günther: Friedrich-Alexander-University, D-91054 Erlangen, Germany
Eva Martini: Friedrich-Alexander-University, D-91054 Erlangen, Germany
Nadine Wittkopf: Friedrich-Alexander-University, D-91054 Erlangen, Germany
Kerstin Amann: Friedrich-Alexander-University, D-91054 Erlangen, Germany
Benno Weigmann: Friedrich-Alexander-University, D-91054 Erlangen, Germany
Helmut Neumann: Friedrich-Alexander-University, D-91054 Erlangen, Germany
Maximilian J. Waldner: Friedrich-Alexander-University, D-91054 Erlangen, Germany
Stephen M. Hedrick: University of California, San Diego, La Jolla, California 92093, USA
Stefan Tenzer: Institute of Immunology, Johannes Gutenberg University, D-55131 Mainz, Germany
Markus F. Neurath: Friedrich-Alexander-University, D-91054 Erlangen, Germany
Christoph Becker: Friedrich-Alexander-University, D-91054 Erlangen, Germany

Nature, 2011, vol. 477, issue 7364, 335-339

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/nature10400

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