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Highly Accessed Review

Transforming growth factor-β-induced regulatory T cells referee inflammatory and autoimmune diseases

Sharon M Wahl1* and Wanjun Chen2

Author Affiliations

1 Cellular Immunology Section, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Disease, National Institutes of Health, Bethesda, Maryland, USA

2 Mucosal Immunology Unit, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Disease, National Institutes of Health, Bethesda, Maryland, USA

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Arthritis Res Ther 2005, 7:62-68  doi:10.1186/ar1504

Published: 24 January 2005

Abstract

Naturally occurring CD4+CD25+ regulatory T cells mediate immune suppression to limit immunopathogenesis associated with chronic inflammation, persistent infections and autoimmune diseases. Their mode of suppression is contact-dependent, antigen-nonspecific and involves a nonredundant contribution from the cytokine transforming growth factor (TGF)-β. Not only can TGF-β mediate cell–cell suppression between the regulatory T cells and CD4+CD25- or CD8+ T cells, but new evidence also reveals its role in the conversion of CD4+CD25- T cells, together with TCR antigen stimulation, into the regulatory phenotype. Elemental to this conversion process is induction of expression of the forkhead transcription factor, Foxp3. This context-dependent coercion of naive CD4+ T cells into a powerful subset of regulatory cells provides a window into potential manipulation of these cells to orchestrate therapeutic intervention in diseases characterized by inadequate suppression, as well as a promising means of controlling pathologic situations in which excessive suppression dominates.