1. IFNγ signaling endows DCs with the capacity to control type I inflammation during parasitic infection through promoting T-bet+ regulatory T cells.
- Author
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Lee HM, Fleige A, Forman R, Cho S, Khan AA, Lin LL, Nguyen DT, O'Hara-Hall A, Yin Z, Hunter CA, Muller W, and Lu LF
- Subjects
- Animals, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Inflammation immunology, Mice, Mice, Knockout, Oligonucleotide Array Sequence Analysis, Real-Time Polymerase Chain Reaction, Signal Transduction immunology, T-Box Domain Proteins immunology, T-Lymphocytes, Regulatory cytology, Th1 Cells cytology, Th1 Cells immunology, Cell Differentiation immunology, Dendritic Cells immunology, Interferon-gamma immunology, T-Lymphocytes, Regulatory immunology, Toxoplasmosis immunology
- 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.
- Published
- 2015
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