IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine

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. Yancopoulos, Carmen J. Booth, Judy H. Cho, Wenjun Ouyang, Clara Abraham and Richard A. Flavell
Additional contact information
Samuel Huber: Yale University School of Medicine
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

Nature, 2012, vol. 491, issue 7423, 259-263

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.

Date: 2012
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DOI: 10.1038/nature11535

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