Author
Listed:
- Samuel Huber
(Yale University School of Medicine
I. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg 20246, Germany)
- Nicola Gagliani
(Yale University School of Medicine)
- Lauren A. Zenewicz
(Yale University School of Medicine)
- Francis J. Huber
(I. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg 20246, Germany)
- Lidia Bosurgi
(Yale University School of Medicine)
- Bo Hu
(Yale University School of Medicine)
- Matija Hedl
(Section of Digestive Diseases, Yale University)
- Wei Zhang
(Section of Digestive Diseases, Yale University School of Medicine)
- William O’Connor
(Yale University School of Medicine)
- Andrew J. Murphy
(Regeneron Pharmaceuticals, Inc.)
- David M. Valenzuela
(Regeneron Pharmaceuticals, Inc.)
- George D. Yancopoulos
(Regeneron Pharmaceuticals, Inc.)
- Carmen J. Booth
(Section of Comparative Medicine, Yale University School of Medicine)
- Judy H. Cho
(Section of Digestive Diseases, Yale University School of Medicine)
- Wenjun Ouyang
(Genentech, Inc., South San Francisco, California 94080, USA)
- Clara Abraham
(Section of Digestive Diseases, Yale University)
- Richard A. Flavell
(Yale University School of Medicine
Howard Hughes Medical Institute)
Abstract
IL-22 is one of the factors that, although important for wound healing, also promote tumorigenesis; the regulation of IL-22BP, the IL-22 binding protein, via the NLRP3 and NLRP6 inflammasomes provides an unanticipated mechanism, controlling IL-22 and thereby the development of colon cancer.
Suggested Citation
Samuel Huber & Nicola Gagliani & Lauren A. Zenewicz & Francis J. Huber & Lidia Bosurgi & Bo Hu & Matija Hedl & Wei Zhang & William O’Connor & Andrew J. Murphy & David M. Valenzuela & George D. Yancopo, 2012.
"IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine,"
Nature, Nature, vol. 491(7423), pages 259-263, November.
Handle:
RePEc:nat:nature:v:491:y:2012:i:7423:d:10.1038_nature11535
DOI: 10.1038/nature11535
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