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

PLoS Pathog 2015 Feb 6;11(2):e1004635. Epub 2015 Feb 6.

Division of Biological Sciences, University of California, San Diego, La Jolla, California, United States of America; Moores Cancer Center, University of California, San Diego, La Jolla, California, United States of America.

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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http://dx.doi.org/10.1371/journal.ppat.1004635DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4450074PMC
February 2015
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