Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of thymic mTEC cells from MyD88fl/fl x Foxn1Cre and MyD88fl/fl mice by transcription profiling

ABSTRACT: Comparison of thymic mTEC cells from MyD88fl/fl x Foxn1Cre and MyD88fl/fl mice by transcription profiling

PROVIDER: PRJEB32958 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR3365970.fastq.gz	Fastqsanger.gz
	ERR3365971.fastq.gz	Fastqsanger.gz
	ERR3365972.fastq.gz	Fastqsanger.gz
	ERR3365973.fastq.gz	Fastqsanger.gz
	ERR3365974.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

E-MTAB-8024

Project description:Comparison of thymic mTEC cells from MyD88fl/fl x Foxn1Cre and MyD88fl/fl mice by transcription profiling

2019-08-08 | E-MTAB-8024 | ExpressionAtlas

Single cell RNA-seq of medullary thymic epithelial cells (mTEC)

Project description:10x sequencing of TSPAN8+, GP2+ or Unselected medullary thymic epithelial cells (mTEC) isolated from female C57BL/6, BALB/c, and C57BL/6 x BALB/c F1 mice with the intent to identify co-expression patterns in promiscuously expressed genes in individual mTEC.

2019-10-17 | E-MTAB-8105 | biostudies-arrayexpress

Aire regulates transfer of antigen from mTEC to dendritic cells for induction of thymic tolerance

Project description:To investigate the role of Aire in thymic selection, we examined the cellular requirements for generation of ovalbumin (OVA)-specific CD4 and CD8 T cells in mice expressing OVA under the control of the rat insulin promoter (RIP). Aire-deficiency reduced the number of mature single positive (SP) OVA-specific CD4+ or CD8+ T cells in the thymus, independent of OVA expression. Importantly, it also contributed in two way to OVA-dependent negative selection depending on the T cell type. Aire-dependent negative selection of OVA-specific CD8 T cells correlated with Aire-regulated expression of OVA. By contrast, for OVA-specific CD4 T cells, Aire affected tolerance induction by a mechanism that operated independent of the level of OVA expression, controlling access of antigen presenting cells to mTEC-expressed OVA. This study supports the view that one mechanism by which Aire controls thymic negative selection is by regulating the indirect presentation of mTEC-derived antigens by thymic dendritic cells. It also indicates that mTEC can mediate tolerance by direct presentation of Aireregulated antigens to both CD4 and CD8 T cells. Total RNA was extracted from medullary thymic epithelial cells isolated from wildtype and Aire-deficient C57BL/6 mice for comparison of gene expression profiles.

2011-04-06 | E-GEOD-28393 | biostudies-arrayexpress

Comparison of thymic mTEC cells from MyD88fl/fl x Foxn1Cre and MyD88fl/fl mice by transcription profiling

Project description:We compared in vitro mTECs-high from MyD88fl/fl x Foxn1Cre and MyD88fl/fl mice: Thymi were enzymaticaly digested, cells were MACS enriched for CD45- fraction, and FACS sorted using BD Influx sorter. mTECs-high were gated as EpCAM+CD11c-Ly51-MHCII+CD80+. Total RNA was isolated using RNeasy Plus Micro Kit (Qiagen). 5 samples per condition were used.

2020-03-20 | E-MTAB-8024 | biostudies-arrayexpress

Aire regulates transfer of antigen from mTEC to dendritic cells for induction of thymic tolerance

2011-04-06 | GSE28393 | GEO

LC-MSMS of the MHC-I immunopeptidome of murine thymic epithelial cells

Project description:Antigen presentation by cortical and medullary thymic epithelial cells (cTEC and mTEC) ensures the formation of a self-restricted and self-tolerant T cell repertoire, respectively. As such, a broad diversity of self-antigens needs to be presented by mTEC to induce T cell’s self-tolerance. Even though the expression and antigen presentation of protein coding genes in mTEC has been abundantly described, little is known of the implication of allegedly noncoding regions of the genome to tolerance induction. In this study, we focused on transposable elements (TE), which have been shown to be highly expressed by mTEC.

2024-04-17 | PXD042241 | Pride

RNA-seq of medullary thymic epithelial cell (mTEC) subsets in inducible Aire-lineage tracing mice

Project description:The goal of the study was to sequence mRNA expression from sorted medullary thymic epithelial cell (mTEC) subsets in inducible Aire-CreERT2.R26-Stopfl-tdTomato lineage tracing mice after a pulse chase. Four cell subsets were sorted 7 days after a single 2mg pulse of tamoxifen administered by oral gavage. 4 biological replicates (1,2,3,4) were collected derived from 12 pooled thymi per replicate. From the DAPI-;CD45-;EpCAM+ TEC pool, cells were sorted as: pre-Aire (MHCIIlo;RFP-), early-Aire (MHCIIhi;RFP-), late-Aire (MHCIIhi;RFP+), and post-Aire (MHCIIlo;RFP+). The data were used to identify differentially expressed genes across the four mTEC subsets to examine mTEC heterogeneity and identify novel mTEC subpopulations.

2018-05-19 | GSE114651 | GEO

Transcriptome analysis of thymic APC subsets, mTECs and thymic DCs in comparison to splenic DCs

Project description:Thymic antigen-presenting cells (APCs), including thymic dendritic cells (t-DCs) and medullary thymic epithelial cells (mTECs) have been described to play a critical role in thymic Treg generation. Our findings could show that both these thymic APCs can induce a more pronounced demethylation of Foxp3 and other Treg-specific epigenetic signature genes in developing Tregs when compared to splenic DCs. In order to elucidate the unique properties of thymic APCs, gene expression profiling was performed in comparison to splenic DCs. Transcriptome analysis of thymic APCs revealed differential expression of costimulatory molecules that could be involved in stable Treg generation. Importantly, both mTEC- and t-DC- induced alloantigen-specific Tregs displayed significantly higher efficacy in prolonging skin allograft acceptance when compared to alloantigen-specific Tregs generated by splenic DCs.

2017-03-15 | GSE67834 | GEO

Single cell RNA-seq of medullary thymic epithelial cells (mTEC)

Project description:Single cell RNA-seq of medullary thymic epithelial cells (mTEC)

| PRJEB33765 | ENA

Ikaros is a principal regulator of Aire+ mTEC homeostasis, thymic mimetic cell diversity, and central tolerance (scRNA seq)

Project description:The zinc-finger transcription factor Ikaros (Ikzf1) modulates key gene expression programs important for hematopoietic development, and coding mutations in IKZF1 are found in patients with immunodeficiency, leukemia, and autoimmunity. While Ikaros has a well-established function in hematopoiesis, its role in other cell types is less well defined. Here, we uncover new functions for Ikaros in thymic epithelial lineage development and show that Ikzf1 expression in medullary thymic epithelial cells (mTECs) is required for both Autoimmune Regulator positive (Aire+) mTEC development and tissue-specific antigen (TSA) gene expression. Accordingly, TEC-specific deletion of Ikzf1 in mice results in a profound decrease in Aire+ mTECs, a global loss of TSA gene expression, and the development of autoimmunity. Moreover, Ikaros shapes thymic mimetic cell diversity and its deletion results in a dramatic expansion of thymic tuft cells and muscle-like mTECs and a loss of other Aire-dependent mimetic populations. Single-cell analysis reveals Ikaros modulates core transcriptional programs in TECs that correlate with the observed cellular changes. Our findings highlight a previously undescribed role for Ikaros in regulating epithelial lineage development and function, and suggest that failed thymic central tolerance could contribute to the autoimmunity seen in humans with IKZF1 mutations.

2023-10-25 | GSE241742 | 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