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.
journal_name
PLoS Pathogjournal_title
PLoS pathogensauthors
Lee HM,Fleige A,Forman R,Cho S,Khan AA,Lin LL,Nguyen DT,O'Hara-Hall A,Yin Z,Hunter CA,Muller W,Lu LFdoi
10.1371/journal.ppat.1004635subject
Has Abstractpub_date
2015-02-06 00:00:00pages
e1004635issue
2eissn
1553-7366issn
1553-7374pii
PPATHOGENS-D-14-01963journal_volume
11pub_type
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