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Status |
Public on Jan 04, 2019 |
Title |
small RNA-Seq of miR-181 deficient Treg cells |
Organism |
Mus musculus |
Experiment type |
Non-coding RNA profiling by high throughput sequencing
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Summary |
The interdependence of selective cues during development of regulatory T (Treg) cells in the thymus and their suppressive function remains incompletely understood. Here we analyzed this interdependence by taking advantage of highly dynamic changes of miR-181a/b-1 during late T-cell development with very high levels of expression during thymocyte selection followed by massive downregulation in the periphery. Loss of miR-181a/b-1 resulted in inefficient de novo generation of Treg cells in the thymus, but simultaneiously permitted homeostatic expansion in the periphery in the absence of competition. Modulation of T-cell receptor (TCR) signal strength in vivo indicated that miR-181a/b-1 controlled Treg cell formation via establishing adequate signaling thresholds. Unexpectedly, miR-181a/b-1-deficient Treg cells displayed elevated suppressive capacity in vivo, in line with elevated levels of CTLA-4 protein, but not mRNA, in thymic and peripheral Treg cells. Therefore, we propose that intrathymic miR-181a/b-1 controls development of Treg cells and imposes a developmental legacy on their peripheral function.
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Overall design |
miR-181a-1/b-1 deficient Treg cells were sorted and sequenced for small RNA. Wild type Treg cells were used as a control. Results were then analyzed for differential expression of micro RNAs. Three biological replicates were analyzed
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Contributor(s) |
Verheyden NA, Winter SJ, Krueger A |
Citation(s) |
30856173 |
Submission date |
Jan 03, 2019 |
Last update date |
Apr 05, 2019 |
Contact name |
Nikita Aaron Verheyden |
E-mail(s) |
nikita.verheyden@kgu.de
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Organization name |
Institute for Molecular Medicine
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Lab |
Krueger Lab
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Street address |
Sandhofstr. 2-4
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City |
Frankfurt am Main |
State/province |
Hessen |
ZIP/Postal code |
60528 |
Country |
Germany |
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Platforms (1) |
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Samples (6)
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Relations |
BioProject |
PRJNA512620 |
SRA |
SRP175078 |