2. Academic Validation
  3. Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation

Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation

  • Immunity. 2007 Mar;26(3):371-81. doi: 10.1016/j.immuni.2007.02.009.
Arian Laurence 1,  Cristina M Tato,  Todd S Davidson,  Yuka Kanno,  Zhi Chen,  Zhengju Yao,  Rebecca B Blank,  Françoise Meylan,  Richard Siegel,  Lothar Hennighausen,  Ethan M Shevach,  John J O'shea
Affiliations

Affiliation

  • 1 Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
PMID: 17363300 DOI: 10.1016/j.immuni.2007.02.009
Abstract

Recent work has identified a new subset of effector T cells that produces interleukin (IL)-17 known as T helper 17 (Th17) cells, which is involved in the pathophysiology of inflammatory diseases and is thought to be developmentally related to regulatory T (Treg) cells. Because of its importance for Treg cells, we examined the role of IL-2 in Th17 generation and demonstrate that a previously unrecognized aspect of IL-2 function is to constrain IL-17 production. Genetic deletion or antibody blockade of IL-2 promoted differentiation of the Th17 cell subset. Whereas STAT3 appeared to be a key positive regulator of RORgammat and IL-17 expression, absence of IL-2 or disruption of its signaling by deletion of the transcription factor STAT5 resulted in enhanced Th17 cell development. We conclude that in addition to the promotion of activation-induced cell death of lymphocytes and the generation of Treg cells, inhibition of Th17 polarization appears to be an important function of IL-2.

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