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Augmenting CAR T Cell Function with LIGHT

ABSTRACT: Augmenting CAR T Cell Function with LIGHT

PROVIDER: PRJNA1005966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25655753.fastq.gz	Fastqsanger.gz
	SRR25655754.fastq.gz	Fastqsanger.gz
	SRR25655755.fastq.gz	Fastqsanger.gz
	SRR25655756.fastq.gz	Fastqsanger.gz
	SRR25655757.fastq.gz	Fastqsanger.gz

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Augmenting CAR T Cell Function with LIGHT

Project description:Chimeric antigen receptor (CAR) T cell therapy has shown remarkable clinical success in the treatment of B-cell acute lymphoblastic leukemia (B-ALL), non-Hodgkin lymphoma (NHL), and multiple myeloma (MM), but its clinical efficacy in other hematologic tumors and solid tumors has been modest. Some of the major challenges that diminish the efficacy of CAR T cells against solid tumors are tumor-associated antigen heterogeneity and the immunosuppressive tumor microenvironment (TME). To overcome these problems, we developed CAR T cells overexpress with LIGHT (TNFSF14), which is a ligand of both LtβR (lymphotoxin beta receptor) on cancer cells and HVEM (herpes virus entry mediator) on immune cells. In addition to the cancer cell-directed cytotoxicity mediated by the CAR T cells themselves, the interaction of LIGHT with LTβR on tumor cells led to antigen-independent killing; moreover, LIGHT also provided immunostimulatory properties to the T cells. Hence, LIGHT-CAR T cells promoted, through multimodal and orthogonal mechanisms, an improved antitumor response through enhanced tumor killing and costimulatory potential. The antigen-independent killing of heterogeneous cancer cells was widely applicable across various cancer cell lines and was mediated by LIGHT CAR T cells in an LTβR-dependent manner. In addition, LIGHT-CAR T cells demonstrated higher proliferative capacity and proinflammatory cytokine secretion than non-LIGHT expressing CAR T cells. Furthermore, LIGHT-CAR T cells conferred significant tumor control and concomitant survival benefit as compared to non-LIGHT CAR T cells in xenograft models of solid tumors with a heterogeneous expression of the target antigen. The application of LIGHT-CAR T cell therapies may provide a novel therapeutic approach to the treatment of solid tumors in the context of antigen-heterogeneous disease thereby preventing outgrowth of antigen-negative populations leading to disease relapse.

2023-08-16 | GSE240974 | GEO

Local radiation enhances systemic CAR T-cell efficacy by augmenting antigen crosspresentation and T-cell infiltration

Project description:Local radiation enhances systemic CAR T-cell efficacy by augmenting antigen crosspresentation and T-cell infiltration

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Enhancing CAR T-cell efficacy against neuroblastoma through MIF inhibition

Project description:Neuroblastoma is a common pediatric extracranial solid tumor, that arises in the developing sympathetic nervous system. Chimeric antigen receptor (CAR) T-cell therapy has demonstrated promising clinical responses, yet its effectiveness in neuroblastoma benefits only a subset of patients. We evaluated the immunosuppressive secretome of neuroblastoma tumoroids that attenuate CAR T-cells function and efficacy. Secreted proteins were collected from tumoroids and identified by shotgun MS.

2025-04-02 | PXD051044 | Pride

Disruption of SUV39H1-mediated H3K9 methylation sustains CAR T cell function

Project description:Disruption of SUV39H1-mediated H3K9 methylation sustains CAR T cell function

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Nr4a transcription factors limit CAR-T cell function in solid tumors

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Local radiation enhances systemic CAR T-cell efficacy by augmenting antigen crosspresentation and T-cell infiltration

Project description:Chimeric antigen receptor (CAR) T-cell therapy targeting CD19 (CART-19) represents a significant advance in the treatment of patients with relapsed or refractory CD19+ B-cell lymphomas. However, a significant portion of patients either relapse or fail to respond. Moreover, many patients have symptomatic disease, requiring bridging radiation therapy (RT) during the period of CAR T-cell manufacturing. To investigate the impact of 1 to 2 fractions of low-dose RT on CART-19 treatment response, we developed a mouse model using A20 lymphoma cells for CART-19 therapy. We found that low-dose fractionated RT had a positive effect on generating abscopal systemic antitumor responses beyond the irradiated site. The combination of RT with CART-19 therapy resulted in additive effects on tumor growth in irradiated masses. Notably, a significant additional increase in antitumor effect was observed in nonirradiated tumors. Mechanistically, our results validate activation of the cyclic guanosine adenosine synthetase/stimulator of interferon genes pathway, tumor-associated antigen crosspriming, and elicitation of epitope spreading. Collectively, our findings suggest that RT may serve as an optimal priming and bridging modality for CAR T-cell therapy, overcoming treatment resistance and improving clinical outcomes in patients with CD19+ hematologic malignancies.

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Project description:We performed transcriptome sequencing on Neo-2/15 stimulated CAR NK cells,to shed light on the function and phenotype changes of CAR-NK cells stimulated by IL-2 and Neo-2/15.

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CAR T cells inhibit B cell activating phosphorylation in their targets

Project description:Adoptive cell therapy, a subset of cancer immunotherapy, is collection of therapeutic approaches which aim to redirect the immune system by reprogramming patient T-cells to target antigenic molecules differentially and specifically expressed in certain cancers. One promising immunotherapy technique is CAR T-cell therapy, where cancer cells are targeted through the expression a chimeric antigen receptor (CAR), a synthetic trans- membrane receptor that functionally compensates for the T-cell receptor (TCR) but targets a tumor associated antigen on the cancer cell surface. While CAR T-cell therapy is promising with two clinically approved second-generation CARs (Kymriah and Yescarta), few studies have investigated the mechanism of signal propagation in T-cells and no studies have investigated the potential signaling response in the target cells. To gain further insight to CAR-based signaling, we stimulated third generation CD19 CAR-expressing Jurkat T-cells by co-culture with SILAC labeled CD19HI Raji B-cells and used two phosphoenrichment strategies coupled with liquid chromatography-tandem mass spec- trometry (LC-MS/MS) to detect and analyze global phosphorylation changes in both cell populations. Analysis of the phosphopeptides originating from the CD19-CAR T cells revealed an increase in many phosphorylation events necessary for canonical TCR signaling. We also observed for the first time a significant decrease in B-cell receptor- related phosphopeptide abundance in CD19HI Raji B-cells after co-culture with CD19-targetted CAR T-cells.

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The role of a novel CAR-induced gene TUBA8 in hepatocellular carcinoma cell lines

Project description:The Tuba8 gene was identified as a CAR-regulated gene that was induced during phenobarbital (PB) promotion of liver tumor. TUBA8 was then over-expressed in heaptocarcinoma cells to determine the function of TUBA8. First, identify genes that are regulated by CAR and are induced during liver tumor development. Second, overexpressiong of an identified gene in transformed cells to detemine the biolgical function of the gene product. In this manuscript, the TUBA8 gene was examined.

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