Article abstract

Nature Immunology 9, 632 - 640 (2008)
Published online: 27 April 2008 | Corrected online: 4 May 2008 | doi:10.1038/ni.1607

A critical function for TGF-bold beta signaling in the development of natural CD4+CD25+Foxp3+ regulatory T cells

Yongzhong Liu1, Pin Zhang1, Jun Li1, Ashok B Kulkarni2, Sylvain Perruche1 & WanJun Chen1

The molecular mechanisms directing the development of 'natural' CD4+CD25+Foxp3+ regulatory T cells (Treg cells) in the thymus are not thoroughly understood. We show here that conditional deletion of transforming growth factor-beta receptor I (TbetaRI) in T cells blocked the appearance of CD4+CD25+Foxp3+ thymocytes at postnatal days 3–5. Paradoxically, however, beginning 1 week after birth, the same TbetaRI-mutant mice showed accelerated expansion of thymic CD4+CD25+Foxp3+ populations. This rapid recovery of Foxp3+ thymocytes was attributable mainly to overproduction of and heightened responsiveness to interleukin 2, as genetic ablation of interleukin 2 in TbetaRI-mutant mice resulted in a complete absence of CD4+CD25+Foxp3+ cells from the thymus and periphery. Thus, transforming growth factor-beta signaling is critical to the thymic development of natural CD4+CD25+Foxp3+ Treg cells.

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  1. Mucosal Immunology Unit, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA.
  2. Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA.

Correspondence to: WanJun Chen1 e-mail: wchen@mail.nih.gov

* In the version of this article initially published online, error bars in Figures 2b, 3b,c, 4b–d, 5b, 7b and 8b were incorrect. The error has been corrected for all versions of the article.

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