Published February 6, 2015
| Version v1
Journal article
Open
IFNγ Signaling Endows DCs with the Capacity to Control Type I Inflammation during Parasitic Infection through Promoting T-bet+ Regulatory T Cells
Creators
- 1. University of California, San Diego
- 2. Technical University Braunschweig
- 3. University of Manchester
- 4. University of Chicago
- 5. University of Pennsylvania
- 6. Jinan University
Description
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.
Data availability
All relevant data are within the paper and its Supporting Information files except for the microarray data which is available from NCBI GEO Datasets under the accession number GSE64594.Files
journal.ppat.1004635.pdf
Files
(5.3 MB)
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Article md5:d7034011b76a0b1c395d59c577c8c2b6 |
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Supporting information md5:65ba9f64ac9cb07224dec52a1a39c684 |
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Additional details
Identifiers
- DOI
- 10.1371/journal.ppat.1004635
- Other
- oai:uchicago.tind.io:8206
Funding
- National Institutes of Health
- R00-AI089935
- Sidney Kimmel Foundation
- Hellman Fellows
- Cancer Research Institute
- Irvington Postdoctoral Fellow
- Deutsche Forschungsgemeinschaft
- SFB 621
- European Network of Excellence
- MUGEN LSHG-CT-2005-005203