Regulatory T cells in inflammatory bowel disease

Boden, Elisa K; Snapper, Scott B

Gastrointestinal Unit and the Center for the Study of Inflammatory Bowel Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA

Correspondence to Scott B. Snapper, MD, PhD, Department of Medicine, Massachusetts General Hospital, 55 Blossom Street, Boston, Massachusetts 02114, USA E-mail:[email protected]

Current Opinion in Gastroenterology24(6):p 733-741, November 2008. |DOI:10.1097/MOG.0b013e328311f26e

Abstract

Purpose of review

The intestinal immune system must orchestrate a complex balance between proinflammatory and anti-inflammatory responses to luminal antigens, and disruptions in this balance can result in inflammatory bowel disease (IBD). This review explores recent data that elucidate the role of regulatory T cells (Tregs) in the pathogenesis of IBD in mice and humans.

Recent findings

Data from murine models of colitis implicate several novel mechanisms critical to Treg function and generation including the inhibitory cytokine interleukin-35, pericellular adenosine generation and cytokine deprivation-induced apoptosis. Although Tregs are essential in mice for the maintenance of intestinal homeostasis, their role in human IBD remains unclear. Patients with IBD appear to have relatively reduced numbers of Tregs in the blood and colon; however, Tregs from these patients are functionalin vitro.

Summary

Tregs are important for the maintenance of intestinal self-tolerance and will likely prove to be an important avenue for therapeutic manipulation in IBD.