Open AccessIFNγ Signaling Endows DCs with the Capacity to Control Type I Inflammation during Parasitic Infection through Promoting T-bet+ Regulatory T Cells
Author(s) -
HyangMi Lee,
Anne Fleige,
Ruth Forman,
Sunglim Cho,
Aly A. Khan,
Ling-Li Lin,
Duc T. Nguyen,
Aisling O’Hara Hall,
Zhinan Yin,
Christopher A. Hunter,
Werner Müller,
Li-Fan Lu
Publication year - 2015
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1004635
Subject(s) - immunology , immune system , biology , dendritic cell , population , inflammation , t cell , regulatory t cell , microbiology and biotechnology , immunity , cytokine , il 2 receptor , medicine , environmental health
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.