Spalinger MR, McCole DF, Rogler G, Scharl M. Protein tyrosine phosphatase non-receptor type 2 and inflammatory bowel disease. World J Gastroenterol 2016; 22(3): 1034-1044 [PMID: 26811645 DOI: 10.3748/wjg.v22.i3.1034]
Corresponding Author of This Article
Michael Scharl, MD, Division of Gastroenterology and Hepatology, University Hospital Zurich, Raemistrasse 100, 8091 Zurich, Switzerland. michael.scharl@usz.ch
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Topic Highlight
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jan 21, 2016; 22(3): 1034-1044 Published online Jan 21, 2016. doi: 10.3748/wjg.v22.i3.1034
Protein tyrosine phosphatase non-receptor type 2 and inflammatory bowel disease
Marianne R Spalinger, Declan F McCole, Gerhard Rogler, Michael Scharl
Marianne R Spalinger, Gerhard Rogler, Michael Scharl, Division of Gastroenterology and Hepatology, University Hospital Zurich, 8091 Zurich, Switzerland
Declan F McCole, Division of Biomedical Sciences, University of California, Riverside (UCR), Riverside, CA 92521, United States
Gerhard Rogler, Michael Scharl, Zurich Center for Integrative Human Physiology, University of Zurich, 8091 Zurich, Switzerland
Author contributions: Spalinger MR, McCole DF, Rogler G and Scharl M solely contributed to this paper.
Supported by Grants from the Swiss National Science Foundation (SNF) to MS, Grant No. 314730-146204 and No. CRSII3_154488/1 (to Rogler G), Grant No. 310030-120312; and the Swiss IBD Cohort, Grant No. 3347CO-108792.
Conflict-of-interest statement: The authors have no conflict of interests to disclose.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Michael Scharl, MD, Division of Gastroenterology and Hepatology, University Hospital Zurich, Raemistrasse 100, 8091 Zurich, Switzerland. michael.scharl@usz.ch
Telephone: +41-44-2559519 Fax: +41-44-2559497
Received: April 21, 2015 Peer-review started: April 23, 2015 First decision: July 20, 2015 Revised: August 31, 2015 Accepted: November 19, 2015 Article in press: November 19, 2015 Published online: January 21, 2016 Processing time: 268 Days and 16.7 Hours
Core Tip
Core tip: Genetic variants and subsequently aberrant function of protein tyrosine phosphatase non-receptor type 2 (PTPN2) have been associated with inflammatory bowel disease (IBD). Protein levels of PTPN2 are increased in the mucosa of IBD patients and PTPN2-deficient mice suffer from severe intestinal as well as systemic inflammation and feature alterations in innate and adaptive immune responses. In the innate immune system, dysfunction of PTPN2 results in increased secretion of pro-inflammatory cytokines, impairs autophagosome formation, and mediates disruption of epithelial barrier function. In the adaptive immune system, PTPN2 is involved in controlling T-cell proliferation, differentiation and promoting T-cell tolerance. Consequently, variants in PTPN2 importantly affect intestinal homeostasis and contribute to IBD pathogenesis.
