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Clinical and Developmental Immunology
Volume 2007 (2007), Article ID 89195, 10 pages
Review Article

Regulatory T Cells and Human Disease

1Vaccine and Infectiouse Disease Institute (VIDI), Laboratory of Experimental Hematology, University of Antwerp, Antwerp 2610, Belgium
2Center for Cellular Therapy and Regenerative Medicine, Antwerp University Hospital, Antwerp 2650, Belgium

Received 16 July 2007; Accepted 8 November 2007

Academic Editor: Yang Liu

Copyright © 2007 Nathalie Cools 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.


The main function of our immune system is to protect us from invading pathogens and microorganisms by destroying infected cells, while minimizing collateral damage to tissues. In order to maintain this balance between immunity and tolerance, current understanding of the immune system attributes a major role to regulatory T cells (Tregs) in controlling both immunity and tolerance. Various subsets of Tregs have been identified based on their expression of cell surface markers, production of cytokines, and mechanisms of action. In brief, naturally occurring thymic-derived CD4+CD25+ Tregs are characterized by constitutive expression of the transcription factor FOXP3, while antigen-induced or adaptive Tregs are mainly identified by expression of immunosuppressive cytokines (interleukin-10 (IL-10) and/or transforming growth factor-β (TGF-β)). While Tregs in normal conditions regulate ongoing immune responses and prevent autoimmunity, imbalanced function or number of these Tregs, either enhanced or decreased, might lead, respectively, to decreased immunity (e.g., with tumor development or infections) or autoimmunity (e.g., multiple sclerosis). This review will discuss recent research towards a better understanding of the biology of Tregs, their interaction with other immune effector cells, such as dendritic cells, and possible interventions in human disease.