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Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [CD8 inducible human RNAseq]

ABSTRACT: Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [CD8 inducible human RNAseq]

PROVIDER: PRJNA1199945 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31758500.fastq.gz	Fastqsanger.gz
	SRR31758501.fastq.gz	Fastqsanger.gz
	SRR31758502.fastq.gz	Fastqsanger.gz
	SRR31758503.fastq.gz	Fastqsanger.gz
	SRR31758504.fastq.gz	Fastqsanger.gz

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Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [Human RNAseq inducible]

Project description:The efficacy of Chimeric Antigen Receptor (CAR) T cells against solid tumors is limited by immunosuppressive factors in the tumor microenvironment (TME) including adenosine, which suppresses CAR T cells through activation of the A2A receptor (A2AR). To overcome this, CAR T cells were engineered to express A1 receptor (A1R), a receptor that signals inversely to A2AR. Using murine and human CAR T cells, constitutive A1R overexpression was demonstrated to significantly enhance CAR T cell effector function albeit at the expense of CAR T cell persistence. Through a novel CRISPR/Cas9 “knock-in” approach we demonstrated that CAR T cells engineered to express A1R in a tumor-localized manner, led to enhanced anti-tumor efficacy dependent on the transcription factor IRF8 and was transcriptionally unique when compared to A2AR deletion. This data provides a novel approach for enhancing CAR T cell efficacy in solid tumors and provides proof of principle for site-directed expression of factors that promote effector T cell differentiation.

2025-03-16 | GSE284618 | GEO

Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [CD8 inducible human RNAseq]

2025-03-16 | GSE284619 | GEO

Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [human ATACseq]

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Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [human RNAseq constitutive]

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Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [Mouse RNAseq constitutive]

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Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [Human RNAseq inducible]

Project description:Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [Human RNAseq inducible]

| PRJNA1199936 | ENA

Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [human ATACseq]

Project description:Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [human ATACseq]

| PRJNA1199942 | ENA

Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [Mouse RNAseq constitutive]

Project description:Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [Mouse RNAseq constitutive]

| PRJNA1199924 | ENA

Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [human RNAseq constitutive]

Project description:Tumor-site directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors. [human RNAseq constitutive]

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NR4a knock-down in HER2 CAR-T cells improves T cell longevity and promotes solid tumor eradication [RNA-Seq]

Project description:Chimeric antigen receptor (CAR)-T cell therapy targeting human CD19 have demonstrated clinical efficacy against B-cell malignancies. However, CAR-T cell therapy's efficacy against solid tumors is limited due to factors like low tumor-associated antigens, infiltration rate, and T cell exhaustion. We have shown that deleting NR4a genes in CAR-T cells prevents T cell exhaustion and improved their therapeutic effects on solid tumors in a mouse model. To further explore this for human, we deleted all three NR4a family factors in CAR-T cells that recognize Epidermal Growth Factor Receptor type 2 (HER2) using the CRISPR/Cas9 system. These modified CAR-T cells (NR4a-TKO CAR-T) exhibited resistance to exhaustion, increased tumor-killing activity, and higher efficacy in tumor regression and survival rate in a human lung carcinoma model in mice. The enhanced therapeutic effects were associated with increased cytokine expression, reduced exhaustion-related gene expression, and improved persistence within tumors. We propose that targeting NR4a could be a promising strategy for developing superior CAR-T cells against solid tumors.

2024-08-28 | GSE241456 | GEO

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