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| Status |
Public on May 01, 2013 |
| Title |
MicroRNA-155 confers encephalogenic potential to Th17 cells by promoting IL-23 responsiveness and effector gene expression |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
|
| Summary |
We examined the role of miR-155 in differentiated Th17 cells during their induction of Experimental Autoimmune Encephalomyelitis (EAE). Using adoptive transfer experiments, we found that highly purified, MOG antigen specific Th17 cells lacking miR-155 are defective in their capacity to cause EAE. Gene expression profiling of purified miR-155-/- IL-17F+ Th17 cells identified a subset of effector genes that are dependent upon miR-155 for their proper expression through a mechanism involving repression of the transcription factor Ets1. Among the genes reduced in the absence of miR-155 was IL-23R, resulting in miR-155-/- Th17 cells being hypo-responsive to IL-23. Taken together, our study demonstrates a critical role for miR-155 in Th17 cells as they unleash autoimmune inflammation, and finds that this occurs through a signaling network involving miR-155, Ets1 and the clinically relevant IL-23-IL-23R pathway.
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| Overall design |
two biological replicates of miR-155-/- CD4+ IL-17F RFP+ T cells compared to two biological replicates of miR-155+/+CD4+IL-17F RFP+ T cells (as a control).
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| Contributor(s) |
Hu R, Huffaker TB, Kagele DA, Runtsch MC, Bake E, Round JL, O'Connell RM |
| Citation(s) |
23686497 |
| |
| Submission date |
Mar 13, 2013 |
| Last update date |
Feb 02, 2018 |
| Contact name |
Brett Milash |
| E-mail(s) |
brett.milash@utah.edu
|
| Organization name |
University of Utah
|
| Department |
Center for High Performance Computing
|
| Street address |
155 S. 1452 E. Room 414
|
| City |
Salt Lake City |
| State/province |
UT |
| ZIP/Postal code |
84112 |
| Country |
USA |
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| Platforms (1) |
| GPL10787 |
Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version) |
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| Samples (4)
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| Relations |
| BioProject |
PRJNA192933 |
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