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Article
Nature Immunology 6, 1142 - 1151 (2005)
Published online: 16 October 2005; Corrected online: 10 March 2006 | doi:10.1038/ni1263


There is an Erratum (April 2006) associated with this Article.

A function for interleukin 2 in Foxp3-expressing regulatory T cells

Jason D Fontenot1, 2, Jeffrey P Rasmussen1, Marc A Gavin1 & Alexander Y Rudensky1

1  Howard Hughes Medical Institute, Department of Immunology, University of Washington, Seattle, Washington 98195, USA.

2  Present address: Laboratory of Lymphocyte Signaling, Rockefeller University, New York, New York 10021, USA.

Correspondence should be addressed to Jason D Fontenot jfontenot@rockefeller.edu or Alexander Y Rudensky aruden@u.washington.edu

Regulatory T cells (Treg cells) expressing the forkhead family transcription factor Foxp3 are critical mediators of dominant immune tolerance to self. Most Treg cells constitutively express the high-affinity interleukin 2 (IL-2) receptor alpha-chain (CD25); however, the precise function of IL-2 in Treg cell biology has remained controversial. To directly assess the effect of IL-2 signaling on Treg cell development and function, we analyzed mice containing the Foxp3 gfp knock-in allele that were genetically deficient in either IL-2 (Il2-/-) or CD25 (Il2ra-/-). We found that IL-2 signaling was dispensable for the induction of Foxp3 expression in thymocytes from these mice, which indicated that IL-2 signaling does not have a nonredundant function in the development of Treg cells. Unexpectedly, Il2-/- and Il2ra-/- Treg cells were fully able to suppress T cell proliferation in vitro. In contrast, Foxp3 was not expressed in thymocytes or peripheral T cells from Il2rg-/- mice. Gene expression analysis showed that IL-2 signaling was required for maintenance of the expression of genes involved in the regulation of cell growth and metabolism. Thus, IL-2 signaling seems to be critically required for maintaining the homeostasis and competitive fitness of Treg cells in vivo.
*Note: In the version of this article initially published, the GEO database accession number is missing. This should be the final subsection of Methods, as follows:

Accession code. GEO: microarray data, GSE4179.

The error has been corrected in the PDF version of the article.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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