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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

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


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.

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