Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mouse CD8+CD122+ regulatory T cells

ABSTRACT: Gene expression profile was compared between CD8+CD122+ T cells and CD8+CD122- T cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE13890 | GEO | 2008/12/31

SECONDARY ACCESSION(S): PRJNA110291

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mouse CD8+CD122+ regulatory T cells

Project description:Gene expression profile was compared between CD8+CD122+ T cells and CD8+CD122- T cells. mRNA taken from CD8+CD122+ cells or CD8+CD122- cells collected by cell sorting from C57BL/6 mice spleen was amplified and analyzed by using gene chip of Agilent.

2008-12-30 | E-GEOD-13890 | biostudies-arrayexpress

Sequence analysis of CD4 Treg, CD8 Treg and CD8 effector

Project description:We show that Ly49+CD122+ CD8+ Treg have a distinct expression profie compared to conventional Foxp3+ CD4+ Treg and CD49 lo CD122+ CD8 effector like cells. RNA was extracted from sorted cells and sent for sequencing

2020-05-16 | GSE150628 | GEO

ADAM17 mediated post-translational regulation of CD122 signaling enhances CD8+ T cell anti-tumor immunity

Project description:CD8+ T cell immune responses are regulated by multi-layer networks, while the post-translational regulations remain largely unknown. Transmembrane ectodomain shedding is an important post-translational process regulating receptor expression and signal transduction by proteolytic cleavage of membrane proteins. Here, by targeting sheddase A Disintegrin and Metalloprotease (ADAM)17, we defined a post-translational regulatory mechanism mediated by ectodomain shedding in CD8+ T cells. Transcriptomic and proteomic analysis revealed the involvement of post-transcriptional/translational regulations in CD8+ T cells. T cell-specific deletion of ADAM17 led to a dramatic increase of effector CD8+ T cell differentiation and enhanced cytolytic effects to eliminate pathogens and tumors. Mechanistically, ADAM17 regulated CD8+ T cells by cleavage of membrane CD122. ADAM17 deficient CD8+ T cells had elevated CD122 expression and response to cytokines IL-2 and IL-15. Intriguingly, inhibition of ADAM17 in CD8+ T cells improved the efficacy of chimeric antigen receptor (CAR) T cells in solid tumor. Our findings reveal a critical post-translational regulation in CD8+ T cells, providing a potential therapeutic strategy of targeting ADAM17 for effective anti-tumor immunity. We then performed gene expression profiling analysis using data obtained from RNA-seq of 10 samples from two groups.

2024-07-20 | GSE236582 | GEO

Microarray data from uterine CD122+ macrophages

Project description:IL-15-responsive CD122+ macrophages (CD122+Macs) develop in the uterus during normal pregnancy. We aimed to understand the signals driving macrophages to adopt this fate. We aimed to determine how CD122+Macs and conventional uterine macrophages differ transcriptionally.

2020-06-08 | GSE132353 | GEO

Expression Data from Memory P14 Tg CD8 T cells after either saline mock-infection, Pichinde Virus Infection (bystander infection) or Pichinde Virus infection with daily treatment with anti-CD122 (clone TM-b1)

Project description:Exposure to inflammatory cytokines driven by bystander cytokines can have profound effects on the function of memory CD8 T cells. Here we transferred a 1-5X10^4 of P14 TCR-tg T cells (specific for gp33-41 of LCMV) on day -1 followed by infection with 2X10^5 PFU of LCMV Armstrong ip to generate memory P14 populations. Mice were rested for >50 days before further challenge. Mice containing memory P14 populations were either mock-infected with saline, infected with 2X10^6 Pichinde Virus ip (no cross-reactivity wtih LCMV gp33-41) or infected with 2X10^6 Pichinde Virus ip together with daily injections of 200 micrograms of anti-CD122 antibody (clone TM-b1). On day 4 following indicated treatments P14s were flow sorted and RNA was extracted from 1X10^6 cells using an RNeasy kit (Qiagen). Each group had 3 biological replicates. Transcriptomes were compared by DAVID analysis (p<0.01, Fold-Change > 1.5) 3 biological replicates per group. Groups included P14 from mock-infected mice, P14 from Pichinde virus infected mice and P14 from Pichinde virus and anti-cd122 treated mice.

2015-09-01 | E-GEOD-69791 | biostudies-arrayexpress

Pandion PT-101 single-cell RNA-seq of CD122+ non-myeloid cells following IL-2 mutein treatment

Project description:This study uses samples from the Pandion Phase 1a IL-2 mutein (PT-101) trial to investigate the mechanism of action of IL-2 mutein therapy. IL-2 mutein is engineered for increased affinity for CD25 and decreased affinity for CD122, selectively activating regulatory T cells (Tregs) while limiting stimulation of CD122-expressing effector populations (NK cells, ILCs, and CD122+ T cells). This dataset addresses whether the highest tested dose (10mg) induces an undesirable, off-target transcriptional signature in CD122+ non-myeloid cells. Single-cell RNA-seq (10x Genomics Chromium) was performed on FACS-sorted CD122+ cells from PBMC of 4 subjects in the 10mg dose cohort, at baseline (pre-treatment) and Day 8 post-dose, to assess treatment-induced changes in cell cluster composition and gene expression at single-cell resolution.

2026-07-30 | GSE338670 | GEO

Stable inhibitory activity of regulatory T cells requires the transcription factor Helios

Project description:The maintenance of immune homeostasis requires regulatory T cells (Tregs). Given their intrinsic self-reactivity, Tregs must stably maintain a suppressive phenotype to avoid autoimmunity. We report that impaired expression of the transcription factor (TF) Helios by FoxP3+ CD4 and Qa-1-restricted CD8 Tregs results in defective regulatory activity and autoimmunity in mice. Helios-deficient Treg develop an unstable phenotype during inflammatory responses characterized by reduced FoxP3 expression and increased effector cytokine expression secondary to diminished activation of the STAT5 pathway. CD8 Treg also require Helios-dependent STAT5 activation for survival and to prevent terminal T cell differentiation. Definition of Helios as a key transcription factor that stabilizes regulatory T-cells in the face of inflammatory responses provides a genetic explanation for a core property of regulatory T-cells. We used microarrays to detail the global programs of gene expression by CD8 Treg (CD44+CD122+Ly49+) and conventional memory type of CD8 cells (CD44+CD122+Ly49-).

2015-09-15 | E-GEOD-73015 | biostudies-arrayexpress

Microarray data from uterine CD122+ macrophages

Project description:Microarray data from uterine CD122+ macrophages

| PRJNA547675 | ENA

ADAM17 mediated post-translational regulation of CD122 signaling enhances CD8+ T cell anti-tumor immunity

Project description:ADAM17 mediated post-translational regulation of CD122 signaling enhances CD8+ T cell anti-tumor immunity

| PRJNA991595 | ENA

Sustained A2AR expression and loss paradoxically promote CD8+ T cell exhaustion

Project description:Although A2AR is a key immunoregulatory receptor that suppresses CD8⁺ T-cell activation in response to elevated extracellular adenosine in inflamed or hypoxic microenvironments, its role in CD8⁺ T cell differentiation and cell-fate decisions during chronic viral infection and cancer remains poorly understood. Using A2AR-eGFP reporter mice, we show that A2AR expression is rapidly induced by TCR stimulation and persists under chronic antigen exposure and hypoxia, with sustained expression strongly associated with terminal exhaustion via the canonical Gαs–cAMP–PKA pathway. Paradoxically, A2AR loss does not alleviate exhaustion but instead accelerates differentiation toward the terminally exhausted state. Single-cell multiomics profiling revealed that A2AR deficiency activates CD122 (IL-2Rβ)–dependent signaling, driving T-cell exhaustion. Genetic deletion of CD122 in A2AR-deficient CD8⁺ T cells reduced terminal exhaustion, identifying CD122 signaling as a key mediator of A2AR loss–driven exhaustion. Intriguingly, both sustained A2AR expression and A2AR loss converge to promote T cell exhaustion differentiation through distinct mechanisms. These findings uncover a paradoxical role of A2AR in shaping CD8⁺ T cell fate choices during chronic infection and cancer.

2026-07-15 | GSE310452 | 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