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

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

PROVIDER: PRJNA786531 | 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 - Targeted Pooled CRISPR Screen for T cell Exhaustion

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

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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

TARGETING NEURONAL FTL1 RESCUES COGNITIVE IMPAIRMENTS IN AGING

Project description:TARGETING NEURONAL FTL1 RESCUES COGNITIVE IMPAIRMENTS IN AGING

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Dynamic chromatin regulatory landscape of human CAR T cell exhaustion [HiChIP]

Project description:Dysfunction in T cells limits the efficacy of cancer immunotherapy. We profiled the epigenome, transcriptome, and enhancer connectome of exhaustion-prone GD2-targeting HA-28z chimeric antigen receptor (CAR) T cells and control CD19-targeting CAR T cells, which present less exhaustion-inducing tonic signaling, at multiple points during their ex vivo expansion. We found widespread, dynamic changes in chromatin accessibility and 3D chromosome conformation preceding changes in gene expression, notably at loci proximal to exhaustion-associated genes such as PDCD1, CTLA4, and HAVCR2, and increased DNA motif access for AP-1 family transcription factors, which are known to promote exhaustion. Although T cell exhaustion has been studied in detail in mouse, we find that the regulatory networks of T cell exhaustion differ between the species and involve distinct loci of accessible chromatin and cis-regulated target genes in human CAR T cell exhaustion. Deletion of exhaustion-specific candidate enhancers of PDCD1 suppress the expression of PD-1 in an in vitro model of T cell dysfunction and in HA-28z CAR T cells, suggesting enhancer editing as a path forward in improving cancer immunotherapy.

2021-05-01 | GSE168881 | GEO

Dynamic chromatin regulatory landscape of human CAR T cell exhaustion [ATAC-seq]

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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.

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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.

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