Tumor-specific CD8+ T cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA949608 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23992213.fastq.gz | Fastqsanger.gz | |||
| SRR23992214.fastq.gz | Fastqsanger.gz | |||
| SRR23992215.fastq.gz | Fastqsanger.gz | |||
| SRR23992216.fastq.gz | Fastqsanger.gz | |||
| SRR23992217.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 28 |
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Project description:scRNA-seq of tumor-specific CD8+ T cells
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Project description:RNA-seq of tumor-specific CD8+ T cells
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Project description:Tumor-specific CD8+ T cells are heterogeneous; Tcf1+ stem-like CD8+ T cells give rise to cytotoxic Tim-3+ terminally differentiated CD8+ T cells. The goal of this study is to determine the capacity of CD69 to regulate differentiation of tumor-specific CD8+ T cells in the tumor microenvironment and tumor-draining lymph nodes. Our single-cell RNA-seq and RNA-seq analyses of tumor-specific CD8+ T cells reveal the important function of CD69 in anti-tumor CD8+ T cell immunity. Thus, CD69 is an attractive target for cancer immunotherapy.
2023-03-29 | GSE228387 | GEO
Project description:Tumor-specific CD8+ T cells are heterogeneous; Tcf1+ stem-like CD8+ T cells give rise to cytotoxic Tim-3+ terminally differentiated CD8+ T cells. The goal of this study is to determine the capacity of CD69 to regulate differentiation of tumor-specific CD8+ T cells in the tumor microenvironment and tumor-draining lymph nodes. Our single-cell RNA-seq and RNA-seq analyses of tumor-specific CD8+ T cells reveal the important function of CD69 in anti-tumor CD8+ T cell immunity. Thus, CD69 is an attractive target for cancer immunotherapy.
2023-03-29 | GSE228386 | GEO
Project description:Gene expression analysis of tumor-specific CD8 T cells encountering a tumor-specific antigen in pre-malignant lesions in the liver at different time points post tumor initiation. The overall goal of this mouse study was to elucidate the molecular program in tumor-specific T cells encountering a tumor-specific antigen in pre-malignant lesions. The study identifies the genes and pathways that are dysregulated in tumor-specific T cells associated with T cell unresponsiveness in tumors. To identify the genes and pathways that are dysregulated in tumor-specific T cells. Gene signatures of the following sample groups were compared: 1. Naïve CD8 T cells; 2. Effector CD8 T cells; 3. Dysfunctional tumor-specific CD8 T cells isolated from pre-malignant lesions 8-12 days after tumor induction. 4. Dysfunctional tumor-specific CD8 T cells isolated from pre-malignant lesions 32-34 days after tumor initiation. The mouse tumor model that was used is an autochthonous, tamoxifen-inducible liver cancer model (ASTxCre-ERT2; AST=Albumin-floxStop-SV40 large T antigen; Cre-ERT2 = TAM-dependent Cre-recombinase) in which the SV40 large T antigen serves as the oncogenic driver and tumor-specific antigen; SV40-I TCR transgenic mice, whose CD8 T cells express a Db-restricted TCR specific for the Tag epitope I were used as source of naïve tumor-specific CD8 T cells (TCRSV40-I) Total RNA was isolated from flow-sorted transgenic CD8 TCRSV40-I T cells from the following sample groups: Naïve, effector, D8-12-pre-malignant lesions, and D32-34 pre-malignant lesions.
2016-08-11 | E-GEOD-60501 | biostudies-arrayexpress
Project description:CD8+ T cell-mediated immune response plays a pivotal role in controlling tumor growth.However, within the tumor microenvironment (TME), prolonged antigen exposure, as well as immunosuppressive factors, drive infiltrated tumor-specific CD8+ T cells into a hyporesponsive state known as “exhaustion”. Notably, our current understanding of tumor-specific CD8+ T cells mainly comes from experiments focusing on tumor infiltrated T cells, less is known about those in tumor draining LNs. Hence, we profiled the chromosome accessibilities of antigen-specific CD8+ T cells from tumor draining LNs of melanoma bearing mice in this project, aiming to draw a comprehensive immune-atlas of tumor-specific CD8+ T cells during tumorigenesis.
2022-10-10 | GSE180084 | GEO
Project description:CD8+ T cell-mediated immune response plays a pivotal role in controlling tumor growth.However, within the tumor microenvironment (TME), prolonged antigen exposure, as well as immunosuppressive factors, drive infiltrated tumor-specific CD8+ T cells into a hyporesponsive state known as “exhaustion”. Notably, our current understanding of tumor-specific CD8+ T cells mainly comes from experiments focusing on tumor infiltrated T cells, less is known about those in tumor draining LNs. Hence, we profiled the chromosome accessibilities of antigen-specific CD8+ T cells from tumor draining LNs of melanoma bearing mice in this project, aiming to draw a comprehensive immune-atlas of tumor-specific CD8+ T cells during tumorigenesis.
2022-10-10 | GSE214384 | GEO
Project description:Gene expression analysis of tumor-specific CD8 T cells encountering a tumor-specific antigen in pre-malignant lesions in the liver at different time points post tumor initiation. The overall goal of this mouse study was to elucidate the molecular program in tumor-specific T cells encountering a tumor-specific antigen in pre-malignant lesions. The study identifies the genes and pathways that are dysregulated in tumor-specific T cells associated with T cell unresponsiveness in tumors. To identify the genes and pathways that are dysregulated in tumor-specific T cells. Gene signatures of the following sample groups were compared: 1. Naïve CD8 T cells; 2. Effector CD8 T cells; 3. Dysfunctional tumor-specific CD8 T cells isolated from pre-malignant lesions 8-12 days after tumor induction. 4. Dysfunctional tumor-specific CD8 T cells isolated from pre-malignant lesions 32-34 days after tumor initiation. The mouse tumor model that was used is an autochthonous, tamoxifen-inducible liver cancer model (ASTxCre-ERT2; AST=Albumin-floxStop-SV40 large T antigen; Cre-ERT2 = TAM-dependent Cre-recombinase) in which the SV40 large T antigen serves as the oncogenic driver and tumor-specific antigen; SV40-I TCR transgenic mice, whose CD8 T cells express a Db-restricted TCR specific for the Tag epitope I were used as source of naïve tumor-specific CD8 T cells (TCRSV40-I)
2016-08-11 | GSE60501 | GEO
Project description:ATAC-seq analysis of tumor-specific CD8 T cells from tumors with and without tumor-specific CD4 T cells
2024-05-19 | GSE265847 | GEO
Project description:Comparison of genome-wide mRNA expresson between tumor-infiltrating CD8+ T cells from the tumor (hypofunctional T cells) and periphery (functional T cells) Mechanisms of self-tolerance often result in CD8+ tumor-infiltrating lymphocytes (TIL) with a hypofunctional phenotype incapable of tumor clearance. Using a solid tumor model in mice, we found that CD8+ T cells became tolerized in less than 24 hours in an established tumor environment. To define the collective impact of pathways suppressing TIL function, we compared genome-wide mRNA expression of tumor-specific CD8+ T cells from the tumor and periphery. Notably, gene expression induced during TIL hypofunction more closely resembled self-tolerance than viral-exhaustion. Differential gene expression was refined to identify a core set of genes that defined hypofunctional TIL; these data comprise the first âmolecular profileâ of tumor-specific TIL that are naturally responding and represent a polyclonal repertoire. The molecular profile of TIL was further dissected to determine the extent of overlap and distinction between pathways that collectively restrict T cell functions. As suggested by the molecular profile of TIL, protein expression of inhibitory receptor LAG-3 was differentially regulated throughout prolonged late-G1/early-S phase of the cell cycle. Our data may accelerate efficient identification of combination therapies to boost anti-tumor function of TIL specifically against tumor cells. 4 samples, 3 biological replicates per group.
2016-04-03 | E-GEOD-79858 | biostudies-arrayexpress