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Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy - Targeted Pooled CRISPR Screen for T cell Exhaustion

ABSTRACT: Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy - Targeted Pooled CRISPR Screen for T cell Exhaustion

PROVIDER: PRJNA786536 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17139600.fastq.gz	Fastqsanger.gz
	SRR17139601.fastq.gz	Fastqsanger.gz
	SRR17139602.fastq.gz	Fastqsanger.gz
	SRR17139603.fastq.gz	Fastqsanger.gz
	SRR17139604.fastq.gz	Fastqsanger.gz

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Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy

Project description:Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy

| PRJNA786531 | ENA

Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy - Targeted Pooled CRISPR Screen for T cell Exhaustion

Project description:Tumor-specific T cells are frequently exhausted by chronic antigenic stimulation. To explore new pathways for reinvigoration of anti-tumor immune functions, we developed a human ex vivo exhaustion model by repetitive antigenic stimulation of primary CD8 T cells. This results in T cells that resemble patient-derived T cells in tumors on a phenotypic and transcriptional level. A pooled targeted CRISPR screen was performed on ex vivo exhausted T cells. The readout was elevated CD107a degranulation after repetitive stimulation (CD107a+ vs CD107- cells after 4h co-culture with peptide loaded tumor cells).

2022-11-07 | GSE190246 | GEO

Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-07 | GSE190247 | GEO

BET bromodomain inhibition rescues PD-1-mediated T cell exhaustion in acute myeloid leukemia

Project description:BET bromodomain inhibition rescues PD-1-mediated T cell exhaustion in acute myeloid leukemia

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Gene expression in self-activating- and non-self-activationg CAR-T cells with CD28 or 4-1BB costimulatory domain.

Project description:We observed self-activation of SKM-CAR-T cells which target novel mesothelioma antigen. CAR-T with CD28 costimulatory domain showed signs of exhaustion while those with 4-1BB costimulatory domain did not. To elucidate molecules responsible for self-activation-induced exhaustion, we performed RNA-seq analysis of SKM-CAR-T cells with CD28 or 4-1BB and CD19-CAR-T cells with CD28 or 4-1BB.

2022-08-19 | GSE211352 | GEO

Single residue in CD28-costimulated CAR-T cells limits long-term persistence and antitumor durability

Project description:Chimeric antigen receptor–T (CAR-T) cell therapies can eliminate relapsed and refractory tumors, but the durability of antitumor activity requires in vivo persistence. Differential signaling through the CAR costimulatory domain can alter the T cell metabolism, memory differentiation, and influence long-term persistence. CAR-T cells costimulated with 4-1BB or ICOS persist in xenograft models but those constructed with CD28 exhibit rapid clearance. Here, we show that a single amino acid residue in CD28 drove T cell exhaustion and hindered the persistence of CD28-based CAR-T cells and changing this asparagine to phenylalanine (CD28-YMFM) promoted durable antitumor control. In addition, CD28-YMFM CAR-T cells exhibited reduced T cell differentiation and exhaustion as well as increased skewing toward Th17 cells. Reciprocal modification of ICOS-containing CAR-T cells abolished in vivo persistence and antitumor activity. This finding suggests modifications to the costimulatory domains of CAR-T cells can enable longer persistence and thereby improve antitumor response.

2020-02-11 | GSE145007 | GEO

Gene expression in self-activating CAR-T cells with CD28 or 4-1BB costimulatory domains.

Project description:We observed self-activation of SKM-CAR-T cells which target novel mesothelioma antigen. CAR-T with CD28 costimulatory domain showed signs of exhaustion while those with 4-1BB costimulatory domain did not. Changes in the gene expression by substituting CD28 co-stimulatory domain to 4-1BB co-stimulatory domain was investigated.

2023-05-28 | GSE231443 | GEO

Genome wide expression profiles (RNAseq) of human CD8+ T cells in resting, activated (CD3+CD28) and PD-1-stimulated cells (CD3+CD28+PD-L1-Fc) at diferent time points

Project description:Background: Binding of the programmed death-1 (PD-1) receptor to its ligands (PD-L1/2) transduces inhibitory signals that promote exhaustion of activated T cells. Blockade of the PD 1 pathway is widely used for cancer treatment, yet the inhibitory signals transduced by PD-1 in T cells remain elusive. Methods: Expression profiles of human CD8+ T cells in resting, activated (CD3+CD28) and PD-1-stimulated cells (CD3+CD28+PD-L1-Fc) conditions were evaluated by RNA-seq. Bioinformatic analyses were used to identify signaling pathways differentially regulated in PD 1-stimulated cells.

2019-05-29 | GSE122149 | GEO

Profiling of Naïve (CD45RA+CD28+), EM (CD45RA-CD28-) and TEMRA (CD45RA+CD28-) CD8+ T cells

Project description:Profiling of Naïve (CD45RA+CD28+), EM (CD45RA-CD28-) and TEMRA (CD45RA+CD28-) CD8+ T cells

| PRJNA530997 | ENA

BET bromodomain inhibition rescues PD-1-mediated T cell exhaustion in acute myeloid leukemia

Project description:We report that the bromodomain and extraterminal domain (BET) inhibitor JQ1 inhibits PD-1 expression in Jurkat T cells, primary T cells, and a T cell exhaustion model. Furthermore, JQ1 dramatically impaired the expression of PD-1 and T cell immunoglobulin mucin-domain-containing-3 (Tim-3), and promoted the secretion of cytokines in T cells from patients with acute myeloid leukemia (AML).

2022-08-16 | GSE205605 | GEO

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