Published online Nov 21, 2015. doi: 10.3748/wjg.v21.i43.12283
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: 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.