Table of Contents
ISRN Inflammation
Volume 2014 (2014), Article ID 928461, 14 pages
Review Article

Role of Th17 Cells in the Pathogenesis of Human IBD

CIBER-EHD, Department of Pharmacology, Center for Biomedical Research (CIBM), University of Granada, Avenida del Conocimiento s/n, Granada, 18100 Armilla, Spain

Received 30 September 2013; Accepted 24 December 2013; Published 25 March 2014

Academic Editors: S. M. Dann, T. Karosi, G. Matteoli, and V. Montinaro

Copyright © 2014 Julio Gálvez. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The gastrointestinal tract plays a central role in immune system, being able to mount efficient immune responses against pathogens, keeping the homeostasis of the human gut. However, conditions like Crohn’s disease (CD) or ulcerative colitis (UC), the main forms of inflammatory bowel diseases (IBD), are related to an excessive and uncontrolled immune response against normal microbiota, through the activation of CD4+ T helper (Th) cells. Classically, IBD was thought to be primarily mediated by Th1 cells in CD or Th2 cells in UC, but it is now known that Th17 cells and their related cytokines are crucial mediators in both conditions. Th17 cells massively infiltrate the inflamed intestine of IBD patients, where they produce interleukin- (IL-) 17A and other cytokines, triggering and amplifying the inflammatory process. However, these cells show functional plasticity, and they can be converted into either IFN-γ producing Th1 cells or regulatory T cells. This review will summarize the current knowledge regarding the regulation and functional role of Th17 cells in the gut. Deeper insights into their plasticity in inflammatory conditions will contribute to advancing our understanding of the mechanisms that regulate mucosal homeostasis and inflammation in the gut, promoting the design of novel therapeutic approaches for IBD.