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Public Library of Science, PLoS Pathogens, 2(11), p. e1004635, 2015

DOI: 10.1371/journal.ppat.1004635

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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

Journal article published in 2015 by Hyang-Mi Lee, Anne Fleige, Ruth Forman, Sunglim Cho, Aly Azeem Khan, Ling-Li Lin, Duc T. Nguyen, Aisling O'Hara-Hall ORCID, Zhinan Yin, Christopher A. Hunter, Werner Muller, Li-Fan Lu
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

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.