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Series GSE112244 Query DataSets for GSE112244
Status Public on Feb 13, 2019
Title Th1 and T17 activation with and without CB839 treatment
Organism Mus musculus
Experiment type Expression profiling by high throughput sequencing
Summary Activated T cells differentiate into functional subsets which require distinct metabolic programs. Glutaminase (GLS) converts glutamine to glutamate to provide substrate for the tricarboxylic acid cycle and epigenetic reactions and here we identify a key role for GLS in T cell activation and specification. Though GLS-deficiency diminished T cell activation, proliferation and impaired differentiation of Th17 cells, loss of GLS also increased Tbet and Interferon-γ expression and CD4 Th1 and CD8 CTL effector cell differentiation. These changes were mediated by differentially altered gene expression and chromatin accessibility, leading to increased sensitivity of Th1 cells to IL-2 mediated mTORC1 signaling. In vivo, GLS-null T cells failed to drive a Th17-mediated Graft-vs-Host Disease model. Transient inhibition of GLS, however, increased Th1 and CTL T cell numbers in viral and chimeric antigen receptor models. Glutamine metabolism thus has distinct roles to promote Th17 but constrain Th1 and CTL effector cell differentiation.
Overall design Cells were treated with glutaminase1 inhibitor or vehicle
Contributor(s) Johnson M, Rathmell J
Citation(s) 30392958
Submission date Mar 23, 2018
Last update date Feb 13, 2019
Contact name Aguirre A de Cubas
Organization name Vanderbilt University Medical Center
Department Hematology and Oncology
Lab Rathmell Lab
Street address 2220 Pierce Ave
State/province TN
ZIP/Postal code 37232
Country USA
Platforms (1)
GPL21493 Illumina HiSeq 3000 (Mus musculus)
Samples (12)
GSM3061549 Th1 + Vehicle 1
GSM3061550 Th1 + Vehicle 2
GSM3061551 Th1 + Vehicle 3
BioProject PRJNA445376
SRA SRP136315

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Supplementary file Size Download File type/resource
GSE112244_MJ308_counts.txt.gz 1.3 Mb (ftp)(http) TXT
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