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Human CAR T cells expressing Super2 and IL-33 retain subset identity

ABSTRACT: Human CAR T cells expressing Super2 and IL-33 retain subset identity

PROVIDER: PRJNA819878 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18477360_1.fastq.gz	Fastqsanger.gz
	SRR18477360_2.fastq.gz	Fastqsanger.gz
	SRR18477361_1.fastq.gz	Fastqsanger.gz
	SRR18477361_2.fastq.gz	Fastqsanger.gz
	SRR18477362_1.fastq.gz	Fastqsanger.gz

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Human CAR T cells expressing Super2 and IL-33 retain subset identity

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TRX1-enhanced CAR T cells retain their antitumor functions under pro-oxidative conditions

Project description:Immunotherapies with CAR-T cells achieve remarkable success, especially against B-cell malignancies. However, their activity against non-hematopoietic solid tumors is very limited. One central cause of this failure may be that a pro-oxidative tumor microenvironment can downmodulate the activation and migration of T-cells. In contrast to tumor cells, primary T cells have very low levels of antioxidants. This makes them prone to pro-oxidative effects. Oxidation-induced dysregulation of actin cytoskeletal dynamics hinders T-cell migration which allows only low tumor infiltration rates. In addition, the proliferation and the effector functions of T-cells (tumor cell killing) are disrupted. In order to strengthen human CAR-T cells against a pro-oxidative tumor microenvironment, we have increased increase their antioxidant capacity, e.g. by expressing antioxidants. We aimed to characterize the importance of antioxidant empowerment at functional level and at the molecular level. Among the antioxidant systems, thioredoxin1 (TRX1)-empowerment, allowed CAR T cells to retain their capacities for cytolytic immune synapse formation, cytokine release, proliferation, and cytotoxicity under pro-oxidative conditions. At the molecular level, gene expression analysis revealed that a pro-oxidative micromilieu caused a downmodulation of costimulatory and cytokine signals of T cells. One unique focus of this study was also to investigate global influence of reactive oxygen species on protein oxidation in T cells. Therefore, using TRX1 kinetic trapping and consequently mass spectrometry was employed to get insight into global oxidation levels in T cells. This analysis, namely redoxosome analysis, unveiled 196 oxidized proteins which were annotated to regulate several antitumor T cell functions. Taken together, our results provide evidence that TRX1 empowerment can increase CAR T cell efficacy against solid tumors.

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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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Placental T cells retain enhanced stemness and altered cytokine response favoring durable efficacy of CD19 CAR-T

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Phenobarbital and TCPOBOP effects on CAR and PXR regulated genes involved in drug metabolism and cholesterol homeostasis

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Reciprocal Transcription Factor Networks Govern Tissue-Resident ILC3 Subset Function and Identity

Project description:Reciprocal Transcription Factor Networks Govern Tissue-Resident ILC3 Subset Function and Identity

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