Article Text

Download PDFPDF
T regulatory cell suppression of colitis: the role of TGF-β
  1. R Duchmann,
  2. M Zeitz
  1. Medizinische Klinik I, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany
  1. Correspondence to:
    Professor R Duchmann
    Medizinische Klinik I, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, D-12200 Berlin, Germany; rainer.duchmann{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Transforming growth factor β (TGF-β) and interleukin 2 may be involved in IBD peripheral regulatory T cell pathophysiology, raising the possibility of therapeutic application of TGF-β induced regulatory T cells in IBD patients

CD4+CD25+ regulatory T cells (Treg) expressing the lineage marker Foxp3 control immune responses to self- and foreign antigens and are an intensely studied member of the heterogenous group of regulatory T cells. Although initially described as a population of suppressor T cells required to avoid organ specific autoimmunity, it has subsequently become clear that Treg control immune responses in a much broader sense, including transplantation tolerance and immune responses to pathogens and tumours.1–3 Relevant to inflammatory bowel diseases (IBD), Treg prevent4 and treat established5 colitis in animal models of IBD and are numerically deficient in patients with active IBD.6 This underlines the fact that the immune dys-equilibrium characteristic of chronic inflammatory diseases involves concomitant disturbances in inflammatory and suppressive immune mechanisms and opens up novel approaches for IBD therapy by strengthening Treg mediated suppression.

Currently, efforts in laboratories worldwide are addressing the central questions of Treg immunology, resolution of which will help us see more clearly the role of Treg in disease pathogenesis and therapy. Some of these central questions are: where do Treg come from; how are they generated, expanded, and maintained; how and where do they function; why do they fail to control immune responses in disease; and how can their therapeutic potential be used most efficiently and safely. As current data indicate that Treg from IBD patients are functionally normal6–8 but numerically deficient during active disease,6 it will be interesting to understand the underlying mechanisms and, based on that knowledge, devise the most promising strategy to enlarge their …

View Full Text


  • Conflict of interest: None declared.

Linked Articles