Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Metabolic signaling directs the reciprocal lineage decisions of αβ and γδ T cells

ABSTRACT: Development of ab and gd T cells requires coupling of environmental signals with metabolic and redox regulation by mTORC1

ORGANISM(S): Mus musculus

PROVIDER: GSE112982 | GEO | 2018/07/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Metabolic signaling directs the reciprocal lineage decisions of αβ and γδ T cells

Project description:The interaction between extrinsic factors and intrinsic signal strength governs thymocyte development, but mechanisms linking them remain elusive. We report that mTORC1 couples microenvironmental cues with metabolic programs in orchestrating reciprocal development of two fundamentally distinct lineages, αβ and γδ T cells. Loss of mTORC1 impairs αβ but promotes γδ T cell development, and disrupts metabolic remodeling of oxidative and glycolytic metabolism. Mechanistically, reactive oxygen species (ROS) controlled by mTORC1 serves as a key metabolic signal, and perturbation of redox homeostasis impinges upon fate decisions. Furthermore, singlecell RNA sequencing and genetic dissection reveal that mTORC1 links developmental signals from T cell receptors and NOTCH to coordinate metabolic activity and signal strength. Our results establish mTORC1-driven metabolic signaling as a fundamental mechanism underlying thymocyte lineage choices. We used microarrays to compare the global transcription profiles of WT and Raptor-null cell populations in DN3a developing thymocytes, immaturesingle-positive (ISP) T-cells, and γδ T-cells

2018-07-06 | GSE86495 | GEO

Metabolic signaling directs the reciprocal lineage decisions of αβ and γδ T cells

Project description:Metabolic signaling directs the reciprocal lineage decisions of αβ and γδ T cells

| PRJNA449676 | ENA

Metabolic signaling directs the reciprocal lineage decisions of ?? and ?? T cells.

Project description: Not available

| S-EPMC6230375 | biostudies-literature

BTN3A1 governs antitumor responses by coordinating αβ and γδ T cells.

Project description: Not available

| S-EPMC7646930 | biostudies-literature

SOX13 regulated genes in CD4+CD8+ double positive thymocytes

Project description:ab and gd T cells originate from a common, multi-potential precursor population in the thymus, but the molecular mechanisms regulating this lineage fate decision process are unknown. We have identified Sox13 as a gd-specific gene in the immune system. Using Sox13 transgenic mice, we show that SOX13 promotes gd T cell development while opposing ab T cell differentiation. Conversely, mice deficient in Sox13 expression exhibited impaired development of gd T cells, but not ab T cells. One mechanism of SOX13 function is the inhibition of WNT/TCF signaling, suggesting that differential WNT/TCF activity is an essential parameter for this binary cell fate choice. Keywords: global gene expression profile comparison

2006-12-20 | GSE6311 | GEO

γδ-T cells and αβ-TCR transduced γδ-T cells

Project description:RNA expression of unstimulated γδ-T cells,γδ-TCR-stimulated γδ-T cells, unstimulated αβ-TCR transduced γδ-T cells and αβ-TCR-stimulated αβ-TCR transduced γδ-T cells.

2023-09-07 | GSE216880 | GEO

A Macrophage Colony-Stimulating Factor-Producing gamma-delta T Cell Subset Prevents Malarial Parasitemic Recurrence

Project description:Despite evidence that gd T cells play an important role during malaria, their precise role remains unclear. During murine malaria induced by Plasmodium chabaudi infection and in human P. falciparum infection, we found that gd T cells expanded rapidly after resolution of acute parasitemia, in contrast to ab T cells that expanded at the acute stage and then declined. Single-cell sequencing showed that TRAV15N-1 gd T cells were clonally expanded in mice and had convergent complementarity-determining region 3 sequences. These gd T cells expressed specific cytokines, M-CSF, CCL5, CCL3, which are known to act on the myeloid compartment, indicating that this gd T cell subset may have distinct functions. Both gd T cells and M-CSF were necessary for preventing parasitemic recurrence. These findings point to an M-CSF-producing gd T cell subset that fulfills a specialized protective role in the later stage of malaria infection when ab T cells have declined.

2018-01-22 | GSE108478 | GEO

γδ T cells shape memory-phenotype αβ T cell populations in non-immunized mice.

Project description: Not available

| S-EPMC6592556 | biostudies-literature

Profiling of mucosal derived bovine ab and gd T cells during Salmonella enterica serovar typhimurium enterocolitis

Project description:gd T cells have an important yet incompletely defined role in inflammation associated with a variety of infectious and autoimmune conditions. To better understand the precise roles of gd T cells relative to ab T cells in a specific infection, we utilized Salmonella Enterica Serovar Typhimurium (S. typhimurium) infection in cattle as it is a leading cause of disease in cattle and closely approximates S. typhimurium-induced enterocolitis in humans. To best represent phenotype and gene expression changes occurring in the gut mucosa early in S. typhimurium infection, gd and ab T cells were collected directly from the mesenteric lymphatic ducts and analyzed by FACS or immediately sorted and processed for microarray analysis. Gene expression profiles were compared at intervals during infection within T cell subsets. The majority of gene expression changes in both subsets occurred 48 hours after infection. In response to S. typhimurium infection there was an increase in expression of several genes in gd T cells which were indicative of activation, proliferation and innate function, whereas in ab T cells gene expression changes suggested a lack of S. typhimurium-specific response. This work represents the first focus on gene expression trends in tissue-derived T lymphocytes in an in vivo model that is highly relevant to human S. typhimurium-induced enterocolitis. Keywords: Comparison of ab and gd T cells in bovine lymphatic fluid time course after salmonella or mock infection

2007-06-30 | GSE3439 | GEO

Raptor/mTORC1-dependent metabolic programming of exit from quiescence underlies T cell activation and fate decisions

Project description:Naïve T cells respond to antigen stimulation by exiting from quiescence into clonal expansion and functional differentiation, but the control mechanism is elusive. Here we describe that Raptor/mTORC1-dependent metabolic reprogramming is a central determinant of this transitional process. Loss of Raptor abrogates T cell priming and Th2 cell differentiation, although Raptor function is less important for continuous proliferation of actively cycling cells. mTORC1 coordinates multiple metabolic programs in T cells including glycolysis, lipid synthesis and oxidative phosphorylation to mediate antigen-triggered exit from quiescence. mTORC1 further links glucose metabolism to the initiation of Th2 differentiation by orchestrating cytokine receptor expression and cytokine responsiveness. Activation of Raptor/mTORC1 integrates T cell receptor (TCR) and CD28 co-stimulatory signals in antigen-stimulated T cells. Our studies identify a Raptor/mTORC1-dependent pathway linking signal-dependent metabolic reprogramming to quiescence exit, and this in turn coordinates lymphocyte activation and fate decisions in adaptive immunity. We used microarrays to explore the gene expression profiles differentially expressed in CD4+ T-cells from wild-type (WT) and CD4(cre) x Raptor(fl/fl) mice before and after stimulation with anti CD3/CD28 antibodies.

2014-01-27 | E-GEOD-51668 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data