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PLoS Pathog. 2015 Feb 6;11(2):e1004635. doi: 10.1371/journal.ppat.1004635. eCollection 2015 Feb.

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

Author information

1
Division of Biological Sciences, University of California, San Diego, La Jolla, California, United States of America.
2
Technical University Braunschweig, Braunschweig, Germany.
3
Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom.
4
Department of Human Genetics, Institute for Genomics and Systems Biology, University of Chicago, Chicago, Illinois, United States of America.
5
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
6
The First Affiliated Hospital, International Imunology Center, The Biomedical Translational Research Institute, Key Laboratory of Molecular Immunology and Antibody Engineering of Guangdong Province, Jinan University, Guangzhou, Guangdong, People's Republic of China.
7
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.

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.

PMID:
25658840
PMCID:
PMC4450074
DOI:
10.1371/journal.ppat.1004635
[Indexed for MEDLINE]
Free PMC Article

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