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BioMed Research International
Volume 2013 (2013), Article ID 286368, 10 pages
http://dx.doi.org/10.1155/2013/286368
Research Article

FOXP3+ T Regulatory Cell Modifications in Inflammatory Bowel Disease Patients Treated with Anti-TNF Agents

1Department of Internal Medicine, Inflammatory Bowel Disease Unit, Complesso Integrato Columbus, Catholic University, Largo Gemelli 8, 00168 Rome, Italy
2Department of Gynaecology, Catholic University, Rome, Italy
3Inflammatory Bowel Disease Unit, IRCCS Clinical Institute Humanitas, Rozzano, Milano, Italy
4Department of Paediatric Haematology/Oncology, IRCCS Bambin Gesù Children’s Hospital, Rome, Italy

Received 30 April 2013; Accepted 8 July 2013

Academic Editor: Silvia Gregori

Copyright © 2013 Luisa Guidi 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.

Abstract

Treg modulation has been hypothesized as one of the mechanisms by which antitumor necrosis factor α (TNFα) agents exert their action in rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). However, data in IBD are still conflicting. We evaluated CD4+CD25+FOXP3+ (Tregs) by flow cytometry in peripheral blood from 32 adult IBD patient before (T0) and after the induction of anti-TNFα therapy (T1). Eight healthy controls (HCs) were included. We also evaluated the number of FOXP3+ cells in the lamina propria (LP) in biopsies taken in a subset of patients and controls. Treg frequencies were significantly increased in peripheral blood from our patients after anti-TNFα therapy compared to T0. T1 but not T0 levels were higher than HC. The increase was detectable only in clinical responders to the treatment. A negative correlation was found among delta Treg levels and the age of patients or disease duration and with the activity score of Crohn’s disease (CD). No significant differences were found in LP FOXP3+ cells. Our data suggest the possibility that in IBD patients the treatment with anti-TNFα may affect Treg percentages and that Treg modifications may correlate with clinical response, but differently in early versus late disease.