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Gene expression profiles of chimeric cytokine receptor-engineered CAR-T cells

ABSTRACT: Gene expression profiles of chimeric cytokine receptor-engineered CAR-T cells

PROVIDER: PRJNA895069 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22070112_1.fastq.gz	Fastqsanger.gz
	SRR22070112_2.fastq.gz	Fastqsanger.gz
	SRR22070113_1.fastq.gz	Fastqsanger.gz
	SRR22070113_2.fastq.gz	Fastqsanger.gz
	SRR22070114_1.fastq.gz	Fastqsanger.gz

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Gene expression profiles of chimeric cytokine receptor-engineered CAR-T cells

Project description:The efficacy of chimeric antigen receptor (CAR)-engineered T cell therapy is suboptimal in most of the cancer types , necessitating further improvement in their therapeutic actions. However, enhancing antitumor T cell response inevitably confers an increased risk of cytokine release syndrome associated with monocyte-derived IL-6 secretion. Thus, a novel approach to simultaneously enhance therapeutic efficacy and safety is warranted. In this study, we developed a chimeric cytokine receptor composed of the extracellular domains of GP130 and IL6RA linked to the transmembrane and cytoplasmic domain of IL-7R mutant that constitutively activate JAK-STAT pathway (G6/7R). CAR-T cells with G6/7R efficiently absorbed and degraded monocyte-derived IL-6 both in vitro and in vivo. The G6/7R-expressing CAR-T cells showed superior expansion and persistence in vivo, which resulted in durable antitumor response in multple tumor models. Our strategy can be widely applicable to CAR-T cell therapy to enhance its efficacy and safety, irrespective of the target antigen.

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Gene expression profiles of CAR-T cells engineered with chimeric cytokine receptors to induce JAK-STAT signaling

Project description:The efficacy of chimeric antigen receptor (CAR)-engineered T cell therapy is insufficient in most cancers. However, enhancing the antitumor T cell response inevitably increases the risk of cytokine release syndrome associated with monocyte-derived IL-6 secretion. In this study, we developed a chimeric cytokine receptor consisting of the extracellular domains of GP130 and IL6RA linked to the transmembrane and cytoplasmic domain of IL-7R mutant (insertion of PPCL) (G6/7R). We also generated a modified receptor with the M452L mutation in the IL7R cytoplasmic domain (G6/7R-M452L). CAR-T cells with G6/7R or G6/7R-M452L efficiently absorbed monocyte-derived IL-6 and induced a superior therapeutic response compared to conventional CAR-T cells. Our strategy can be broadly applied to CAR-T cell therapy to enhance its efficacy and safety, irrespective of the target antigen.

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Gene expression profiles of CAR-T cells engineered with chimeric cytokine receptors to induce JAK-STAT signaling

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Gene expression profile of canine Chimeric Antigen Receptor (CAR) Engineered invariant Natural Killer T (iNKT) cells

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Expression data from chimeric antigen receptor transduced (CAR) human CD4+ T cells during expansion

Project description:In this data set we include expression data from human CD4+ T cells isolated on day 0, 6, 11 and 24 follow anti-CD3/anti-CD28 magnetic bead stimulation and chimeric antigen receptor transduction. 30 samples were submitted. Samples represented three biological replicates of normal donors transduced with various CARs. CARs used were a cMet 28z specific CAR comprised of the IgG4 hinge, CD28 transmembrane and CD28 and CD3zeta intracellular domains. A CD19 CD28 CAR was specific to CD19, and was comprised of a CD8a hinge, CD28 transmembrane and CD28 and CD3zeta intracellular domain. A third CAR, the CD19 BBz, was used that was specific to CD19 was comprised of a CD8a hinge, CD8a transmembrane and 4-1BB and CD3zeta intracellular domains. Expression data was analyzied on day 0, 6, 11 and 24.

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Gene expression profile of canine Chimeric Antigen Receptor (CAR) Engineered invariant Natural Killer T (iNKT) cells

Project description:Gene expression profile of canine Chimeric Antigen Receptor (CAR) Engineered invariant Natural Killer T (iNKT) cells

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High affinity chimeric antigen receptor signaling induces an inflammatory program in human regulatory T cells

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