Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expressions of TCRαβ+ CD8αα+ intraepithelial lymphocyte (IELs) in the small intestine with or without Rbpj gene

ABSTRACT: cDNA microarray data of TCRαβ+ CD8αα+ IELs in the small intestine with or without Rbpj gene

ORGANISM(S): Mus musculus

PROVIDER: GSE117122 | GEO | 2019/06/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expressions of TCRαβ+ CD8αα+ intraepithelial lymphocyte (IELs) in the small intestine with or without Rbpj gene

Project description:Gene expressions of TCRαβ+ CD8αα+ intraepithelial lymphocyte (IELs) in the small intestine with or without Rbpj gene

| PRJNA481164 | ENA

BCL6 is required for the thymic development of TCRαβ+CD8αα+ intraepithelial lymphocyte lineage

Project description:TCRαβ+CD8αα+ intraepithelial lymphocytes (CD8αα+ αβ IELs), a specialized subset of T cells in the gut epithelium, develop from thymic agonist-selected IEL precursors (IELps). The molecular mechanisms underlying the selection and differentiation of this T cell type in the thymus are largely unknown. Here, we found that Bcl6 deficiency in αβ T cells resulted in nearly the absence of CD8αα+ αβ IELs. BCL6 was expressed by approximately 50% of CD8αα+ αβ IELs but the majority thymic PD1+ IELps post agonist selection; its deficiency blocked early IELp generation in the thymus. Moreover, BCL6 expression in IELps was induced by thymic TCR signaling in an ERK-dependent manner. As a result of Bcl6 deficiency, the precursors of IELps among CD4+CD8+ double positive (DP) thymocytes exhibited increased apoptosis during agonist selection, and impaired IELp differentiation and maturation. Taken together, our results elucidate BCL6 as a crucial transcription factor during the thymic development of CD8αα+ αβ IELs.

2024-02-26 | GSE248163 | GEO

Kdm6b is required for the maturation and function of intestinal TCRβ+CD8αα+ intraepithelial lymphocytes

Project description:To under the role of Kdm6b in the regulation of intestinal TCRβ+CD8αα+ intraepithelial lymphocytes (IELs), Kdm6b was conditionally deleted in mouse T cells. Small intestinal TCRβ+CD8αα+ IELs were sorted by flow cytometry and RNA-seq was conducted to identify the differentially expressed genes.

2022-08-02 | GSE154444 | GEO

BCL6 is required for the thymic development of TCRαβ+CD8αα+ intraepithelial lymphocyte lineage

Project description:BCL6 is required for the thymic development of TCRαβ+CD8αα+ intraepithelial lymphocyte lineage

| PRJNA1041854 | ENA

Genome-wide maps of chromatin state in mouse small intestinal intraepithelial lymphocytes.

Project description:We performed CUT&Tag-Seq against histone H3K27me3 in mouse small intestinal TCRβ+CD8αα+ intraepithelial lymphocytes (IELs) of wild-type mice to analyze epigenetic modifications.

2022-08-02 | GSE185798 | GEO

Examining the role of murine norovirus (MNV)-infection on intraepithelial lymphocytes (IELs).

Project description:We examined how MNV-infection affects the population and function of IELs in vivo.

2022-07-01 | GSE204822 | GEO

Comprehensive proteomics analyses of IL-15 driven activation of intestinal intraepithelial lymphocytes

Project description:Intestinal intraepithelial lymphocytes (IEL) are an abundant population of tissue-resident T cells that protect the gut from pathogens and maintain intestinal homeostasis. The cytokine IL-15 is trans-presented by epithelial cells to IEL in complex with the IL-15 receptor α chain (IL-15Rα) and plays essential roles both in maintaining IEL homeostasis, and in inducing IEL activation in response to epithelial stress. When overproduced, IL-15 is a key driver of the gluten-induced enteropathy Coeliac disease, through cytotoxic activation of IEL. To better understand how IL-15 directly regulates both homeostatic and inflammatory functions of IEL, we performed quantitative proteomics of IL-15/Rα-stimulated murine IEL, sorted into their 3 main subpopulations, TCRγδ CD8αα, TCRαβ CD8αβ and TCRαβ CD8αα expressing IEL. The data reveal that high IL-15/Rα stimulation licenses cell cycle activation, upregulates the biosynthetic machinery in IEL, increases mitochondrial respiratory capacity and induces expression of cell surface immune receptors and adhesion proteins that potentially drive IEL activation.

2021-05-10 | PXD025891 | Pride

Single cell gene expression analysis of mouse CD45.2+ intraepithelial lymphocyes (IELs) from stomach, small intestine, cecum and colon.

Project description:To understand the diversity of IELs in the gastrointestinal tract, CD45.2+ IELs from stomach, small intestine, cecum and colon of C57BL/6 mice were isolated for single cell RNA sequencing.

2023-10-06 | GSE202690 | GEO

Tissue adaptation is the dominant driver of the proteomic landscape of intestinal intraepithelial lymphocytes

Project description:Intestinal intraepithelial T lymphocytes (T-IEL) patrol the single layer of epithelial cells lining the gut, and consist of both induced T-IEL, derived from systemic antigen-experienced lymphocytes, and natural IEL, that are developmentally targeted to the intestine. To gain functional insights into these enigmatic cells, we used high-resolution quantitative mass spectrometry to investigate the proteomic landscape of the main T-IEL populations in the gut. Comparing the proteomes of induced T-IEL, tissue-resident memory TCRαβ+ CD8αβ+ cells and natural TCRγδ+ CD8αα+ and TCRαβ+ CD8αα+ T-IEL, with naive CD8+ T cells from lymph nodes reveals striking similarities between T-IEL subsets and the dominant effect of the gut environment on T-IEL phenotypes. Analysis of copy numbers/cell of >7000 proteins provides new understanding of the differences in composition of T cell antigen receptor signal transduction pathways in T-IEL versus conventional T cells and reveals skewing of the metabolic machinery towards an exhausted T cell phenotype adapted to the intestinal environment. This study provides a resource for exploring and understanding how multiple inputs are integrated into T-IEL function.

2021-03-15 | PXD023140 | Pride

GPR18 is required for a normal CD8αα intestinal intraepithelial lymphocyte compartment.

Project description:Intraepithelial lymphocytes (IELs) play an important role in maintaining the physiology of the small intestine. The majority of mouse IELs express CD8αα and are either γδ or αβ T cells. Although the development and homing of CD8αα IELs have been studied in some detail, the factors controlling their homeostasis and positioning are incompletely understood. Here we demonstrate that G protein-coupled receptor 18 (GPR18) is abundantly expressed in CD8αα IELs and that mice lacking this orphan receptor have reduced numbers of γδT IELs. Mixed bone marrow chimera experiments reveal a markedly reduced contribution of GPR18-deficient cells to the CD8αα IEL compartment and a reduction in the CD8αβ T cell subset. These defects could be rescued by transduction with a GPR18-expressing retrovirus. The GPR18-deficient γδT IELs that remained in mixed chimeras had elevated Thy1, and there were less granzyme B(+) and Vγ7(+) cells, indicating a greater reduction in effector-type cells. Flow cytometric analysis indicated GPR18 deficiency more strongly affected the CD8αα cells in the intraepithelial compared with the adjacent lamina propria compartment. These findings establish a requirement for GPR18 in CD8αα and CD8αβ IELs, and we suggest the receptor has a role in augmenting the accumulation of CD8 T cells in the intraepithelial versus lamina propria compartment.

| S-EPMC4235638 | biostudies-literature

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