Topic Highlight
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Nov 21, 2015; 21(43): 12283-12295
Published online Nov 21, 2015. doi: 10.3748/wjg.v21.i43.12283
Th17 plasticity and its changes associated with inflammatory bowel disease
Aito Ueno, Abhisek Ghosh, Daniel Hung, Ji Li, Humberto Jijon
Aito Ueno, Daniel Hung, Humberto Jijon, Department of Medicine, University of Calgary, Calgary T2N 1N4, Alberta, Canada
Abhisek Ghosh, Darent Valley Hospital, Dartford, DA2 8DA Kent, United Kingdom
Ji Li, Department of Gastroenterology, Peking Union Hospital, Beijing 100730, China
Author contributions: The listed authors solely contributed to this manuscript in writing and searching the literatures
Conflict-of-interest statement: The authors have no conflict of interest to report in this work.
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:
Correspondence to: Dr. Aito Ueno, Department of Medicine, University of Calgary, HSC1838, 2500 University Dr. NW, Calgary T2N 1N4, Alberta, Canada.
Telephone: +1-403-2206603 Fax: +1-403-2109157
Received: June 23, 2015
Peer-review started: June 26, 2015
First decision: July 20, 2015
Revised: August 17, 2015
Accepted: October 23, 2015
Article in press: October 26, 2015
Published online: November 21, 2015
Core Tip

Core tip: Recently, two innovative clinical failures in inflammatory bowel disease which sought to manipulate T helper (Th) subsets via either transplantation of regulatory T cells or interleukin-17 blockade using secukinumab, suggest that altering the balance between inflammatory and regulatory subsets in inflammatory bowel diseases (IBD) may be more complex than previously thought. One reason may be the flexible nature of T helper subset commitment, otherwise referred to as plasticity. Here we discuss plasticity between regulatory and inflammatory subsets in T helper CD4+ cells, especially Th17 cell subset, and the potential to therapeutically target this process in human IBD.