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Consequences of the perivascular niche remodeling for tumoricidal T-cell trafficking into metastasis of ovarian cancer [Spatial Transciptomics]

ABSTRACT: Consequences of the perivascular niche remodeling for tumoricidal T-cell trafficking into metastasis of ovarian cancer [Spatial Transciptomics]

PROVIDER: PRJNA1146899 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30204207.fastq.gz	Fastqsanger.gz
	SRR30204208.fastq.gz	Fastqsanger.gz
	SRR30204209.fastq.gz	Fastqsanger.gz
	SRR30204210.fastq.gz	Fastqsanger.gz
	SRR30204211.fastq.gz	Fastqsanger.gz

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Consequences of the perivascular niche remodeling for tumoricidal T-cell trafficking into metastasis of ovarian cancer [scRNA-seq]

Project description:Consequences of the perivascular niche remodeling for tumoricidal T-cell trafficking into metastasis of ovarian cancer [scRNA-seq]

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Consequences of the perivascular niche remodeling for tumoricidal T-cell trafficking into metastasis of ovarian cancer [Spatial Transciptomics]

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Consequences of the perivascular niche remodeling for tumoricidal T-cell trafficking into metastasis of ovarian cancer [scRNA-seq]

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Trogocytosis contributes tumor escape and limits tumoricidal activity in hPSCs-derived CAR macrophages

Project description:Pluripotent stem cells (PSCs) derived chimeric antigen receptor macrophages (iCAR-Ms) hold great potential for immunotherapy, particularly against T-cell malignancies which are challenging in CAR-T therapy. Here, we generate human iCAR-Ms targeting CD5 for treating T-cell malignancies. iCAR-Ms display tumoricidal activities against various T- malignant cells expressing CD5 such as Jurkat, SUP-T1 and primary tumor cells. However, The iCAR-M tumoricidal activities are largely dependent on CD5 density on tumor cells. The escaped tumor cells show reversible CD5 loss without changes on its mRNA level. Meanwhile, the retrieved iCAR-Ms show little reduced tumoricidal activities against new tumor cells expressing CD5. Based on time lapse imaging and transcriptional analysis, we show that iCAR-Ms mainly medicate trogocytosis while less phagocytosis when approach tumor cells. Our data reveal trogocytosis as an important limitation factor in iCAR-M tumoricidal activities and tumor escape, providing a rational to develop enhanced CAR-M for immunotherapies.

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Project description:Glioblastoma stem cells (GSCs) have been reported to be found near the blood vessels. We wanted to identify the perivascular GSCs by combining the label retention approach with vascular perfusion. GSCs, like most of the stem cells, are in a quiescent state. Label retention approach involves staining the cells with a uniform membrane labeling dye (PKH26) and allowing them to grow in vivo in NOD SCID mice. Slow-dividing stem cells will retain the dye to a greater extent and perivascular cells are identified by injecting the mice with vascular perfusion dye (Hoechst 33342) 5 min prior to sacrifice. Perivascular GSCs (positive for Hoechst 33342 and pKH26 dye - dubbed as H+P+) were compared with the rest of the perivascular glioma cells (H+P-).

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Project description:The tumoricidal effects of CD8+T cells are well acknowledged, but how MHC Ib-restricted CD8+T (Ib-CD8+T) cells contribute to anti-tumor immunity remains obscure. Here, we show that infusion of MHC Ia+ cells to Kb-/-Db-/- mice induced the expansion of Ib-CD8+T cells in tumors and potently inhibited tumor progression. Such priming of Ib-CD8+T cells by MHC-Ia is not MHC haplotype restricted and MHC Ia tetramers alone can prime Ib-CD8+T cells for activation. The MHC Ia priming promoted Tbet expression in Ib-CD8+T cells and in absence of Tbet, such priming effect diminished. Importantly, these tumoricidal Ib-CD8+T cells are positive for CX3CR1, and exhibit rapid proliferation, high expression of cytotoxic factors, and prolonged persistence at tumor sites. Adoptive transfer of CX3CR1+Ib-CD8+T cells to wild type mice resulted in potent anti-tumor effects. Our findings unravel an uncharacterized function of MHC Ia molecules in immunoregulation and raise the possibility of using Ib-CD8+T cells in tumor immunotherapy.

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