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| Status |
Public on May 22, 2020 |
| Title |
The microRNA miR-22 represses T helper 17 cell pathogenicity by targeting PTEN-regulated pathways |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Multiple sclerosis is a chronic autoimmune disease driven by pathogenic Th17 cells. Here, we dissected the role of miR-22 in pathogenic Th17 cells by autoantigen-specific disease models. We first showed that miR-22 was upregulated in peripheral lymphoid organs and spinal cords of mice developed autoimmune encephalomyelitis. Although miR-22 was upregulated in multiple helper T cell subsets, it was dispensable for T helper cell differentiation in vitro. While miR-22-/- mice exhibited milder symptoms of disease in an active EAE model, adoptive transfer of miR-22-/- 2D2 Th17 cells into naive recipient mice promoted higher disease incidence and severity compared to mice transferred with control 2D2 Th17 cells. Global transcriptional analysis of miR-22-deficient pathogenic Th17 cells revealed upregulated genes in phosphatase and tensin homologue (PTEN)-mediated pathways, and Pten was further identified as one of its potential targets. Therefore, we identified that Th17 cell intrinsic-miR-22 could protect mice from autoimmunity by targeting PTEN-regulated pathways.
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| Overall design |
RNA-seq for Mir-22 wild-type and knock-out in Th17 (23) cells with 3 replicates.
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| Contributor(s) |
Wang L, Qiu R, Zhang Z, Han Z, Yao C, Hou G, Dai D, Jin W, Tang Y, Yu X, Shen N |
| Citation(s) |
32518131 |
| Submission date |
Jul 25, 2019 |
| Last update date |
Aug 21, 2020 |
| Contact name |
Zhijun Han |
| E-mail(s) |
hangeneral@126.com
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| Organization name |
Southern University of Science and Technology
|
| Street address |
No 1088,xueyuan Rd., Nanshan District
|
| City |
Shenzhen |
| State/province |
Guangdong |
| ZIP/Postal code |
518055 |
| Country |
China |
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| Platforms (1) |
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| Samples (6)
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| Relations |
| BioProject |
PRJNA556698 |
| SRA |
SRP216410 |
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