[HTML][HTML] IFNγ signaling endows DCs with the capacity to control type I inflammation during parasitic infection through promoting T-bet+ regulatory T cells

HM Lee, A Fleige, R Forman, S Cho, AA Khan… - PLoS …, 2015 - journals.plos.org
HM Lee, A Fleige, R Forman, S Cho, AA Khan, LL Lin, DT Nguyen, A O'Hara-Hall, Z Yin…
PLoS pathogens, 2015journals.plos.org
IFNγ signaling drives dendritic cells (DCs) to promote type IT 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 …
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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