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Nat Immunol. 2016 Nov;17(11):1322-1333. doi: 10.1038/ni.3540. Epub 2016 Sep 5.

An essential role for the IL-2 receptor in Treg cell function.

Author information

1
Howard Hughes Medical Institute and Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
2
Immunology Discovery, Biogen, Cambridge, MA, USA.
3
Herbert Irving Comprehensive Cancer Center, Department of Pathology and Cell Biology, and Department of Microbiology and Immunology, Columbia University, New York, NY, USA.
4
Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, La Jolla, CA, USA.
5
Institute for Medical Microbiology and Hygiene, University of Mainz Medical Centre, Mainz, Germany.
6
Exploratory Biology, Juno Therapeutics, Seattle, WA, USA.
#
Contributed equally

Abstract

Regulatory T cells (Treg cells), which have abundant expression of the interleukin 2 receptor (IL-2R), are reliant on IL-2 produced by activated T cells. This feature indicates a key role for a simple network based on the consumption of IL-2 by Treg cells in their suppressor function. However, congenital deficiency in IL-2R results in reduced expression of the Treg cell lineage-specification factor Foxp3, which has confounded experimental efforts to understand the role of IL-2R expression and signaling in the suppressor function of Treg cells. Using genetic gain- and loss-of-function approaches, we found that capture of IL-2 was dispensable for the control of CD4+ T cells but was important for limiting the activation of CD8+ T cells, and that IL-2R-dependent activation of the transcription factor STAT5 had an essential role in the suppressor function of Treg cells separable from signaling via the T cell antigen receptor.

PMID:
27595233
PMCID:
PMC5071159
DOI:
10.1038/ni.3540
[Indexed for MEDLINE]
Free PMC Article

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