Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cystine Restriction Alleviates T Cell Exhaustion and Enhances CAR-T Cell Potency

ABSTRACT: This study was designed to explore how targeting Slc7a11 affected CD8+ T cell differentiation and function using a mouse colorectal cancer model. Single-cell RNA-seq was used to monitor tumor-infiltrating CD8+ T cells from Slc7a11 knockout and wild-type mouse tumor models treated with IgG control or anti-Ctla4 antibody.

ORGANISM(S): Mus musculus

PROVIDER: GSE333187 | GEO | 2026/07/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cystine Restriction Alleviates T Cell Exhaustion and Enhances CAR-T Cell Potency

Project description:This study was designed to explore how targeting Slc7a11 affected CD8+ T cell differentiation and function using a mouse colorectal cancer model. TCR-seq was used to profile T cell receptor repertoires in mouse tumor-infiltrating T cells from wild-type and Slc7a11 knockout tumor models treated with IgG control or anti-Ctla4 antibody.

2026-07-18 | GSE333188 | GEO

Leukemia stem cells defend ferroptosis by controlling cystine uptake via PIEZO1-HIF1A-SLC7A11 axis

Project description:Metabolism reprogramming is intimately accompanied with mitochondrial oxidative stress in driving many human diseases including cancers. Excessive oxidative stress frequently induces cell death including ferroptosis, which needs to be tightly balanced for maintaining cellular homeostasis. However, the precise mechanisms for balancing metabolic reprogramming and oxidative stress under different contexts remain elusive. Here, by studying acute myeloid leukemia stem cells (LSCs) that are largely fueled by OXPHOS, we reveal a defense system of LSCs against oxidative stress-induced ferroptosis. We find that the mechano-sensor PIEZO1 plays key role in promoting acute myeloid leukemia development and maintaining LSCs stemness. PIEZO1 deletion impairs cystine uptake and induces ROS and lipid peroxidation, causing ferroptosis of leukemia cells. Mechanistically, HIF1A mediates the function of PIEZO1 by transcriptionally regulating the expression of SLC7A11 and SLC3A2. Further, inhibition of PIEZO1 and SLC7A11 suppresses LSC function and contributes to AML treatment. In summary, our findings reveal that LSCs control cystine uptake through PIEZO1-HIF1A-SLC7A11 axis to defend ferroptosis, representing a unique vulnerability of LSCs.

2026-07-15 | GSE313852 | GEO

MYC-HCC treated with immunotherapy

Project description:Murine MYC-HCC were treated with control IgG or anti PDL1 or anti CTLA4, or their combination. Tumors were sequenced using Nanostring IO360.

2023-02-01 | GSE215006 | GEO

MTOR-dependent expression of SP1 promotes the tolerogenic function of dendritic cells by inducing IL10 expression

Project description:Dendritic cells (DCs) are central regulators of immune responses and tolerance. Although CTLA4-Ig has been reported to promote tolerogenic properties in DCs, the molecular mechanisms underlying this process remain incompletely understood. The aim of this study was to characterize the transcriptional programs associated with CTLA4-Ig-induced tolerogenic DCs. Human monocyte-derived DCs from healthy donors were stimulated with LPS in the presence of either control IgG or CTLA4-Ig and subjected to RNA sequencing. Comparative transcriptomic analysis was performed to identify differentially expressed genes and pathways associated with CTLA4-Ig-mediated tolerogenic reprogramming.

2026-06-25 | GSE335844 | GEO

CTLA4-Ig changed the gene expression associated with cellular movement in osteoclast precursors

Project description:To explore comprehensive gene expression changes, we performed an RNA sequence analysis of CX3CR1-EGFP+ cells from calvaria in mice treated with CTLA4-Ig or control IgG.

2018-05-06 | GSE112896 | GEO

Targeting LRBA triggers CTLA4 degradation and antitumor immunity for cancer immunotherapy

Project description:The lipopolysaccharide-responsive beige-like anchor protein (LRBA) deficiency causes severe autoimmune diseases and cytotoxic T-lymphocyte-associated protein 4 (CTLA4) loss in humans. However, the impact of LRBA on antitumor immunity remains understudied. Here, we identified the role of LRBA in antitumor immunity and developed a novel immunotherapy for cancers. Interestingly, LRBA was negatively associated with antitumor immunity in human patients. Using high-throughput screening and subsequent structure-based hit optimization, we discovered a small molecule LC427 that bound directly to LRBA, and selectively interfered with the LRBA-CTLA4 interaction. This mechanistically unique LC427 facilitated the lysosomal degradation of CTLA4, and bolstered survival and functions of activated T cells. Importantly, orally administrated LC427 increased tumor-infiltrating CD8+ T cells and displayed effective antitumor activity in tumor-bearing mouse models. Notably, LC427 did not induce typical irAEs observed with immune checkpoint inhibitors in colitis models. Our study demonstrates that targeting LRBA offers a novel and effective strategy with a favorable safety profile, highlighting the potential of LRBA-based immunomodulatory therapies in the treatment of cancers.

2026-01-23 | PXD064363 | Pride

The expression of MHC class II molecules on murine breast tumors delays T cell exhaustion, expands the T cell repertoire and slows tumor growth

Project description:Transfection with the human class II transcriptional activator (hCIITA) promotes MHCII expression on TS/A breast cancer cells. Using a murine breast tumor line, we showed that MHCII-expressing tumors grew more slowly than controls and recruited more functional CD4+ and CD8+ T cells. Additionally, MHCII-expressing tumors contained more TCR clonotypes expanded to a larger degree than control tumors. Functional CD8+ T cells in tumors depended on CD4+ T cells. However, both CD4+ and CD8+ T cells eventually became exhausted, even in MHCII-expressing tumors. Treatment with anti-CTLA4, but not anti-PD-1 or anti-TIM-3, promoted complete eradication of MHCII-expressing tumors. These results suggest tumor cell expression of MHCII facilitates the local activation of CD4+ T cells, indirectly helps the activation and expansion of CD8+ T cells and, in combination with the appropriate checkpoint inhibitor, promotes tumor regression.

2018-09-08 | GSE119670 | GEO

TRAM deletion attenuates monocyte exhaustion and alleviates sepsis severity.

Project description: Not available

| S-EPMC10756061 | biostudies-literature

Transcriptome differences in HCC infiltrated CD8+ T cells in effector and exhaustion state

Project description:CD8+ T cells isolated from HCC tissue were divided into three groups: PD1-TIM3- CD8+ TILs, exhibiting full effector function; PD1-intTIM3+ CD8+ TILs, exhibiting partial exhaustion; and PD1-hiTIM3+ CD8+ TILs, exhibiting severe exhaustion, as reflected by the differences in their ability to produce effector cytokines respectively. Transcriptome sequence analysis was performed to investigate the gene expression profile was performed.

2019-12-31 | E-MTAB-7278 | biostudies-arrayexpress

Direct regulation of T cell exhaustion by NFAT [ChIP-Seq]

Project description:During persistent antigen stimulation, CD8+ cytolytic T cells (CTL) show a gradual decrease in effector function, or “exhaustion”, which impairs the immune response to tumors and infections. Here we show that NFAT, a transcription factor with an established role in T cell activation, in parallel controls a second transcriptional program conferring the characteristic features of CD8+ T cell exhaustion, including upregulation of genes encoding inhibitory cell surface receptors and diminished TCR signaling. Expression of an engineered NFAT1, which induces this negative regulatory program in the absence of the effector program, interferes with the ability of CD8+ T cells to protect against Listeria infection or attenuate tumor growth in vivo. NFAT elicits this second program of gene expression in large part by binding to a subset of the sites occupied by NFAT during a typical effector response, suggesting that a balance between the two pathways determines the outcome of TCR signaling. Determination of NFAT1 binding sites in CD8 T cells in vitro

2015-02-13 | E-GEOD-64407 | biostudies-arrayexpress

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