Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA METHYLATION DURING αβ T CELL DEVELOPMENT IN THE HUMAN THYMUS [expression]

ABSTRACT: Thymocyte differentiation is a complex process which involves well-defined sequential developmental stages that finally result in the generation of mature αβ and γδ T cells. Here, we analyzed DNA methylation and gene expression profiles at successive human thymus developmental stages from early T-cell progenitors to single positive (SP) CD4+ and CD8+ subpopulations

ORGANISM(S): Homo sapiens

PROVIDER: GSE54996 | GEO | 2014/12/30

SECONDARY ACCESSION(S): PRJNA238557

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

DNA METHYLATION DURING αβ T CELL DEVELOPMENT IN THE HUMAN THYMUS [methylation]

Project description:Thymocyte differentiation is a complex process which involves well-defined sequential developmental stages that finally result in the generation of mature αβ and γδ T cells. Here, we analyzed DNA methylation and gene expression profiles at successive human thymus developmental stages from early T-cell progenitors to single positive (SP) CD4+ and CD8+ subpopulations

2014-12-30 | GSE55111 | GEO

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

TCR signal strength controls thymic differentiation of discrete proinflammatory γδT cell subsetsistinct TCR signal strength requirements in the thymus

Project description:The murine thymus produces discrete γδ T cell subsets making either IFN-γ or IL-17, but the role of the TCR in this developmental process remains controversial. Here we generated a non-transgenic and polyclonal model of reduced TCR expression and signal strength selectively on γδ T cells. Mice haploinsufficient for both CD3γ and CD3δ (CD3DH) showed normal αβ thymocyte subsets but specific defects in γδ T cell development, namely impaired differentiation of IL-17-producing embryonic Vγ6+ (but not adult Vγ4+) γδ T cells and a marked depletion of IFN-γ-producing CD122+ NK1.1+ (Vγ1-biased) γδ T cells throughout life. As result, adult CD3DH mice showed defective peripheral IFN-γ responses and were resistant to experimental cerebral malaria. Thus, strong TCR signaling is required within specific developmental windows with distinct Vγ usage and differential cytokine production by effector γδ T cell subsets.

2016-03-29 | GSE71637 | GEO

Transcriptional Regulation by NFATc1 during murine thymocyte development [gammadelta_T_cells RNA-seq]

Project description:In thymus hematopoietic precursor cells differentiate into αβ T cells, γδ T cells, mucosa-associated invariant T cells (MAIT), and natural killer T (NKT) cells. We show that both ablation of NFATc1 or its induction during the DN stages of thymocyte development leads to an almost normal thymocyte development but a marked increase in γδ T cells. The γδ cells deficient for NFATc1 acquire an NKT γδ cell phenotype that exhibits the expression of CD4 co-receptor, the NK1.1 marker, the augmented usage of the Vγ1.1 and Vδ6.3 segments, and an increased in IL4 and IFN-γ production.

2023-02-28 | GSE198030 | GEO

Transcriptional Regulation by NFATc1 during murine thymocyte development [BirA RNA-seq]

2023-02-28 | GSE198029 | GEO

Transcriptional Regulation by NFATc1 during murine thymocyte development [ChIP-seq]

2023-02-28 | GSE198028 | GEO

Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development [BCL11B_ex vivo]

Project description:Notch-dependent BCL11B induction converts thymus seeding precursor cells into committed T cell progenitors that subsequently differentiate into T cells bearing either the γδ or αβ T cell receptor. In human, strong Notch activation favors γδ T cell development at the expense of αβ-lineage differentiation, but the underlying molecular mechanism has remained unclear. Therefore, we performed paired mRNA and miRNA profiling across 11 stages of human T cell development, including developing γδ T cells. We identify the miR-17-92 cluster as a direct Notch target and show that miR-17 promotes human TCRγδ T cell development by targeting BCL11B, a gene required for αβ but not for γδ T cell development. Thus, following its role as a licensing factor to induce BCL11B expression in early T cell precursors, Notch activation limits BCL11B expression through miR-17 until thymocytes have passed the β-selection checkpoint when Notch activation is turned off. Hereby Notch prevents premature BCL11B upregulation that is required for αβ-lineage differentiation and this results in preferential γδ-lineage differentiation. Our work unravels a dual role for Notch in controlling BCL11B expression during intrathymic differentiation and provides a unique resource for understanding the mRNA/miRNA interactions that control human T cell development. We used microarrays in order to profile the gene expression in 11 ex vivo T cell subsets, isolated from human thymus. Cord blood CD34+Lin- HPCs were used as a reference subset for extrathymic HPCs.

2020-05-26 | GSE129852 | 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

Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development [BCL11B_coculture]

Project description:Notch-dependent BCL11B induction converts thymus seeding precursor cells into committed T cell progenitors that subsequently differentiate into T cells bearing either the γδ or αβ T cell receptor. In human, strong Notch activation favors γδ T cell development at the expense of αβ-lineage differentiation, but the underlying molecular mechanism has remained unclear. Therefore, we performed paired mRNA and miRNA profiling across 11 stages of human T cell development, including developing γδ T cells. We identify the miR-17-92 cluster as a direct Notch target and show that miR-17 promotes human TCRγδ T cell development by targeting BCL11B, a gene required for αβ but not for γδ T cell development. Thus, following its role as a licensing factor to induce BCL11B expression in early T cell precursors, Notch activation limits BCL11B expression through miR-17 until thymocytes have passed the β-selection checkpoint when Notch activation is turned off. Hereby Notch prevents premature BCL11B upregulation that is required for αβ-lineage differentiation and this results in preferential γδ-lineage differentiation. Our work unravels a dual role for Notch in controlling BCL11B expression during intrathymic differentiation and provides a unique resource for understanding the mRNA/miRNA interactions that control human T cell development. We used microarrays in order to profile gene expression in CD34+ thymocytes before culture and after 5 or 10 days culture on OP9 stromal cells expressing Notch ligands JAG1, JAG2, DLL1 or DLL4.

2020-05-26 | GSE129853 | GEO

Distinct Notch1 and BCL11B requirements mediate human γδ/αβ T cell development [miRNA BCL11B_coculture]

Project description:Notch-dependent BCL11B induction converts thymus seeding precursor cells into committed T cell progenitors that subsequently differentiate into T cells bearing either the γδ or αβ T cell receptor. In human, strong Notch activation favors γδ T cell development at the expense of αβ-lineage differentiation, but the underlying molecular mechanism has remained unclear. Therefore, we performed paired mRNA and miRNA profiling across 11 stages of human T cell development, including developing γδ T cells. We identify the miR-17-92 cluster as a direct Notch target and show that miR-17 promotes human TCRγδ T cell development by targeting BCL11B, a gene required for αβ but not for γδ T cell development. Thus, following its role as a licensing factor to induce BCL11B expression in early T cell precursors, Notch activation limits BCL11B expression through miR-17 until thymocytes have passed the β-selection checkpoint when Notch activation is turned off. Hereby Notch prevents premature BCL11B upregulation that is required for αβ-lineage differentiation and this results in preferential γδ-lineage differentiation. Our work unravels a dual role for Notch in controlling BCL11B expression during intrathymic differentiation and provides a unique resource for understanding the mRNA/miRNA interactions that control human T cell development. The expression of 756 miRNAs was determined using the Taqman stem-loop RT-qPCR method as previously described (Mets E. Leukemia. 2015, Mavrakis KJ. Nat Genet. 2011).

2020-05-26 | GSE129855 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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