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Transforming growth factor-β controls T helper type 1 cell development through regulation of natural killer cell interferon-γ

Authors
  • Laouar, Yasmina1
  • Sutterwala, Fayyaz S1, 2
  • Gorelik, Leonid1, 3
  • Flavell, Richard A1, 4
  • 1 Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, 06520, USA , New Haven (United States)
  • 2 Section of Infectious Diseases, Yale University School of Medicine, New Haven, Connecticut, 06520, USA , New Haven (United States)
  • 3 Biogen Idec, Inc., Cambridge, Massachusetts, 02142, USA , Cambridge (United States)
  • 4 The Howard Hughes Medical Institute, New Haven, Connecticut, 06520, USA , New Haven (United States)
Type
Published Article
Journal
Nature Immunology
Publisher
Springer Nature
Publication Date
Apr 24, 2005
Volume
6
Issue
6
Pages
600–607
Identifiers
DOI: 10.1038/ni1197
Source
Springer Nature
License
Yellow

Abstract

Interferon-γ and interleukin 12 produced by the innate arm of the immune system are important regulators of T helper type 1 (TH1) cell development, but signals that negatively regulate their expression remain controversial. Here we show that transforming growth factor-β (TGF-β) controlled TH1 differentiation through the regulation of interferon-γ produced by natural killer (NK) cells. Blockade of TGF-β signaling in NK cells caused the accumulation of a large pool of NK cells secreting copious interferon-γ, responsible for TH1 differentiation and protection from leishmania infection. In contrast, blockade of TGF-β signaling in dendritic cells did not affect dendritic cell homeostasis or interleukin 12 production, thus indicating a previously undescribed demarcation of the function of TGF-β in NK cells versus dendritic cells.

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