Table of Contents
ISRN Gastroenterology
Volume 2012 (2012), Article ID 505432, 6 pages
Clinical Study

In Crohn's Disease, Anti-TNF- 𝜢 Treatment Changes the Balance between Mucosal IL-17, FOXP3, and CD4 Cells

1Immune Response Unit, Department of Vaccination and Immune Protection, National Institute for Health and Welfare, Haartmaninkatu 8, 00290 Helsinki, Finland
2Division of Gastroenterology, Department of Medicine, Helsinki University Hospital, Haartmaninkatu 4, 00290 Helsinki, Finland
3Children's Hospital, University of Helsinki, Stenbäckinkatu 11, 00290 Helsinki, Finland

Received 27 March 2012; Accepted 18 April 2012

Academic Editors: Y. Araki, J. M. Pajares, and C.-T. Shun

Copyright © 2012 Veera Hölttä et al. 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.


Aim. In Crohn's disease (CD), anti-TNF-α treatment is a potent medication. We aimed to characterize the effect of anti-TNF-α treatment on T effector and regulatory cells. Material and Methods. We studied T-effector and regulatory cells on cellular and mRNA levels in intestinal biopsy samples from 13 Crohn's disease patient. Biopsies were obtained at baseline and 3 months after anti-TNF-α treatment, and from 14 inflammation-free control subjects. Results. Patients had higher numbers of ileal IL-17+ and forkhead box P3 (FOXP3)+ cells than did control subjects, both before ( 𝑃 ≀ 0 . 0 0 1 and 𝑃 ≀ 0 . 0 5 , resp.) and after the anti-TNF-α treatment ( 𝑃 ≀ 0 . 0 1 , 𝑃 ≀ 0 . 0 1 ). Intestinal interferon-γ and IL-17 mRNA expression was higher in Crohn's disease and remained elevated after anti-TNF-α treatment. The ratio of IL-17+ cells to CD4+ cells decreased ( 𝑃 ≀ 0 . 0 5 ) and compared to baseline the ratio of IL-17+ cells to FOXP3+ was lower after treatment ( 𝑃 ≀ 0 . 0 5 ). Conclusions. TNF-α-blocking agents improved intestinal balance between IL-17+ T-effector and regulatory T cells, although intestinal IL-17 upregulation remained elevated.