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IFNγ Signaling Endows DCs with the Capacity to Control Type I Inflammation during Parasitic Infection through Promoting T-bet+ Regulatory T Cells

  • Author(s): Lee, HM
  • Fleige, A
  • Forman, R
  • Cho, S
  • Khan, AA
  • Lin, LL
  • Nguyen, DT
  • O'Hara-Hall, A
  • Yin, Z
  • Hunter, CA
  • Muller, W
  • Lu, LF
  • et al.

Published Web Location

http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004635
No data is associated with this publication.
Abstract

© 2015 Lee et al. IFNγ signaling drives dendritic cells (DCs) to promote type I T cell (Th1) immunity. Here, we show that activation of DCs by IFNγ is equally crucial for the differentiation of a population of T-bet+ regulatory T (Treg) cells specialized to inhibit Th1 immune responses. Conditional deletion of IFNγ receptor in DCs but not in Treg cells resulted in a severe defect in this specific Treg cell subset, leading to exacerbated immune pathology during parasitic infections. Mechanistically, IFNγ-unresponsive DCs failed to produce sufficient amount of IL-27, a cytokine required for optimal T-bet induction in Treg cells. Thus, IFNγ signalling endows DCs with the ability to efficiently control a specific type of T cell immunity through promoting a corresponding Treg cell population.

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