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Transcriptomic profile of Traf6-deficient CD8+ TILs

ABSTRACT: Transcriptomic profile of Traf6-deficient CD8+ TILs

PROVIDER: PRJNA922497 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23035122_1.fastq.gz	Fastqsanger.gz
	SRR23035122_2.fastq.gz	Fastqsanger.gz
	SRR23035123_1.fastq.gz	Fastqsanger.gz
	SRR23035123_2.fastq.gz	Fastqsanger.gz
	SRR23035124_1.fastq.gz	Fastqsanger.gz

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Transcriptomic profile of Traf6-deficient CD8+ TILs

Project description:Transcriptomic profile of sorted CD8+ TILs from Rag1-/- mice 4 days after transferred. Each group has two replicates.

2023-12-06 | GSE222539 | GEO

Transcription profiling of mouse CD8 T cells from two mouse strains (OTI-WT and OTI-TRAF6 knockout) at two timepoints

Project description:CD8 T cells play a crucial role in immunity to infection and cancer. They are maintained in constant numbers, but upon stimulation with antigen undergo a developmental program characterized by distinct phases encompassing the expansion and then contraction of antigen-specific populations, followed by the persistence of long-lived memory cells. Although this predictable pattern of a CD8 T cell response is well established, the underlying cellular mechanisms regulating the transition to memory remain undefined. Here we show that TRAF6, an adapter protein in the TNF-receptor (TNFR) and IL-1R/TLR superfamily, regulates CD8 T cell memory development following infection by modulating fatty acid metabolism. We show that mice with a T cell-specific deletion of TRAF6 mount robust primary CD8 T cell effector responses, but have a profound defect in their ability to generate memory. This defect is CD8 T cell intrinsic and is characterized by the disappearance of antigen-specific cells in the weeks following primary immunization. Microarray analyses revealed that TRAF6-deficient CD8 T cells from early timepoints following immunization exhibit altered expression of genes that regulate fatty acid metabolism. Consistent with this, activated CD8 T cells lacking TRAF6 are unable to upregulate mitochondrial Î²-oxidation in response to growth factor withdrawal in vitro. Treatment with drugs that induce fatty acid oxidation enabled CD8 T cell memory generation in the absence of TRAF6. Remarkably, these treatments also increased CD8 T cell memory in wild type mice, and consequently were able to significantly improve the efficacy of an experimental anti-cancer vaccine. Experiment Overall Design: CD8 T cells from two mouse strains (OTI-WT and OTI-TRAF6 knockout) at two timepoints (6d with 3 replicates and 10d with 5 replicates) after infection are used.

2009-06-24 | E-GEOD-15750 | biostudies-arrayexpress

Global gene expression profile of CD8+ TILs from WT and B7S1 KO mice

Project description:Global gene expression profile of CD8+ TILs from WT and B7S1 KO mice

| PRJNA433480 | ENA

Global gene expression profile of CD8+ TILs from WT and B7S1 KO mice

Project description:B7S1 negatively regulates T cells and its expression correlates with poor prognosis of cancer patients. In order to understand how B7S1 signaling contributes to dysfunction of CD8+ T cell in the TME, we conducted transcriptional analysis of OVA-specific CD8+ TILs and different TIL subsets from E.G7-bearing WT and B7S1 KO mice (Day 21).

2018-04-03 | GSE110249 | GEO

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

Proteome profile of Traf6-OE OT-I T cells

Project description:Proteome profile of Traf6-OE OT-I T cells and EV OT-I cells after viral transfection

2025-05-06 | PXD039327 | Pride

CD8+ TILs in NSCLC differentiate into TEMRA via a bifurcated trajectory, deciphering immunogenicity of tumor-antigens

Project description:CD8+ tumor-infiltrating lymphocytes (TILs) comprise phenotypically and functionally heterogeneous subpopulations. Of these, effector memory CD45RA-expressing CD8+ T cells (Temra) have been discovered and characterized as the most terminally differentiated subset. However, their exact ontogeny and physiological importance in association with tumor progression remain poorly understood. We analyzed primary tumors and peripheral blood samples from 26 patients with non-small cell lung cancer and analyzed their phenotypes and functional characteristics using flow cytometry, RNA-sequencing, and bioinformatics. We found that tumor-infiltrating Temra (tilTemra) cells largely differ from peripheral blood Temra (pTemra), with distinct transcriptomes and functional properties. Notably, although majority of the pTemra was CD27-CD28- double-negative (DN), a large fraction of tilTemra population was CD27+CD28+ double-positive (DP), a characteristic of early-stage, less differentiated effector cells. Trajectory analysis revealed that CD8+ TILs undergo a divergent sequence of events for differentiation into either DP or DN tilTemra. Such a differentiation toward DP tilTemra relied on persistent expression of CD27 and CD28 and was associated with weak T cell receptor engagement. Thus, a higher proportion of DP Temra was correlated with lower immunogenicity of tumor antigens and consequently lower accumulation of CD8+ TILs. These data suggest a complex interplay between CD8+ T cells and tumors and define DP Temra as a unique subset of tumor-specific CD8+ TILs that are produced in patients with relatively low immunogenic cancer types, predicting immunogenicity of tumor antigens and CD8+ TIL counts, a reliable biomarker for successful cancer immunotherapy.

2021-09-14 | GSE184053 | GEO

The Tumor Microenvironment Imposes Persistent ATF4 in CD8+ TILs to Obstruct Cancer Control

Project description:The T cell-intrinsic element that responds to tumor microenvironment (TME) stress to shape CD8+ tumor infiltrating lymphocyte (TIL) fate and function in solid cancers remains elusive. Here we report that the hypoxic TME imprints persistent activity of the central transcriptional node of the integrated stress response (ISR), activating transcription factor 4 (ATF4), in CD8+ TILs that results in metabolic polarity, mitochondrial oxidative stress, and cell death. Chronic ATF4 expression replicated the terminal exhaustion cell state in CD8+ T cells and high Atf4 expression in bulk tumor or peripheral T cells of patients with melanoma predicted poor response to PD-1 inhibition. Genetic or pharmacologic attenuation of ATF4 reduced mitochondrial oxidative stress and promoted viability among CD8+ TILs, enabling complete responses to PD-1 inhibition and conferring protection from re-emergent disease. Our multidisciplinary approach identifies chronic ATF4 activity as a barrier to immune checkpoint inhibitors, positioning ISR therapeutics as novel treatment strategies to improve efficacy of immunotherapy combinations.

2025-06-23 | GSE300172 | GEO

Characterization of gene expression of tumor infiltrating T cells (TILs) in previously untreated patients with follicular lymphoma (FL) compared with those of tonsils

Project description:It has been shown that tumor infiltrating immune cells have a profound impact on the outcome of FL. To find mechanisms whereby TILs are altered gene expession analysis of highly pure TILs were performed. The study is composed of 4 groups, FL CD4 (n=12), FL CD8 (n=9), Tonsil CD4 (n=7) and Tonsil CD8 (n=7). All FL patients were treatment naive. Cells were flowsorted from cryopreserved single cell suspensions and purity of cells were at least 95%.

2013-02-07 | E-GEOD-27928 | biostudies-arrayexpress

Expression data for CD8 TILs subpopulations sorted by Tim3 and PD1

Project description:Reversing the dysfunctional T cell state that arises in cancer and chronic viral infections is the focus of therapeutic interventions; however, current therapies are effective in only some patients and some tumor types. To gain a deeper molecular understanding of the dysfunctional T cell state, we analyzed population and single-cell RNA profiles of CD8+ tumor-infiltrating lymphocytes (TILs) and used genetic perturbations to identify a distinct gene module for T cell dysfunction that can be uncoupled from T cell activation. This distinct dysfunction module is downstream of intracellular metallothioneins that regulate zinc metabolism and can be identified at single-cell resolution. We further identify Gata-3, a zinc-finger transcription factor in the dysfunctional module, as a regulator of dysfunction, and use CRISPR/Cas9 genome editing to show that it drives a dysfunctional phenotype in CD8+ TILs. Our results open novel avenues for targeting dysfunctional T cell states, while leaving activation programs intact.

2016-09-07 | GSE85947 | GEO

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