|
| Status |
Public on Aug 30, 2016 |
| Title |
Gene expression of Glut1 transgenic and control iTreg |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
Effector (Teff) and regulatory (Treg) CD4 T cells undergo metabolic reprogramming to support proliferation and immune function. While Phosphatidylinositide 3-kinase (PI3K)/Akt/mTORC1 signaling induces the glucose transporter Glut1 and aerobic glycolysis for Teff proliferation and inflammatory function, mechanisms that regulate Treg metabolism and function remain unclear. We show that TLR signals that promote Treg proliferation increase Glut1, PI3K/Akt/mTORC1 signaling, and glycolysis. However, TLR-induced mTORC1 signaling also impaired Treg suppressive capacity. Conversely, FoxP3 opposed PI3K/Akt/mTOR signaling to reduce glycolysis and anabolic metabolism while increasing oxidative and catabolic metabolism. Importantly, Glut1 expression was sufficient to increase Treg numbers but reduced suppressive capacity and FoxP3 expression. Thus, inflammatory signals and FoxP3 balance mTORC1 signaling and glucose metabolism to control Treg proliferation and suppressive function.
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| |
|
| Overall design |
RNAseq of induced Glut1 transgenic and control Treg
|
| |
|
| Contributor(s) |
Rathmell J, De Cubas A |
| Citation(s) |
27695003 |
| |
| Submission date |
Jul 27, 2016 |
| Last update date |
May 15, 2019 |
| Contact name |
Jeffrey C Rathmell |
| E-mail(s) |
jeff.rathmell@vanderbilt.edu
|
| Organization name |
Vanderbilt University Medical Center
|
| Street address |
1161 21st Avenue South, A-5301 MCN
|
| City |
Nashville |
| State/province |
Tennessee |
| ZIP/Postal code |
37232-2363 |
| Country |
USA |
| |
|
| Platforms (1) |
| GPL21493 |
Illumina HiSeq 3000 (Mus musculus) |
|
| Samples (9)
|
|
| Relations |
| BioProject |
PRJNA335637 |
| SRA |
SRP079992 |
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