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Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity II

ABSTRACT: Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity II

PROVIDER: PRJNA794177 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17431455.fastq.gz	Fastqsanger.gz
	SRR17431456.fastq.gz	Fastqsanger.gz
	SRR17431457.fastq.gz	Fastqsanger.gz
	SRR17431458.fastq.gz	Fastqsanger.gz
	SRR17431459.fastq.gz	Fastqsanger.gz

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Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity

Project description:Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity

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Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity V

Project description:Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity V

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Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity IV

Project description:Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity IV

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Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity III

Project description:Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity III

| PRJNA794186 | ENA

Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity

Project description:Single cell sequence (SC-seq) has been used to explore the effect of IL10/CSF1R fusion protein modulation in tumor microenvironment. Four groups were analyzed which contain Ctrl, CSF1R, IL10 and BF10. MTC-Q1 oral cancer cells were orthotopic injection in C57BL/6 mice. CD45+ immune cells has been isolated, analyzed and sequenced by dropped based scRNA-seq, cDNA were sequenced by Illumina Novaseq 6000.

2023-07-09 | GSE190111 | GEO

Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity IV

Project description:Bulk RNA sequence (RNA-seq) has been used to explore the effect of IL10/CSF1R fusion protein modulation in tumor microenvironment. Four groups were analyzed which contain Ctrl, CSF1R, IL10 and BF10. MTC-Q1 oral cancer cells were orthotopic injection into C57BL/6J mice. tumor tissue has been isolated (~ 100 mm3) and total RNA were extracted by Trizol, followed by cDNA were sequenced by Illumina NovaSeq6000.

2023-07-09 | GSE193051 | GEO

Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity III

Project description:Bulk RNA sequence (RNA-seq) has been used to explore the effect of IL10/CSF1R fusion protein modulation in tumor microenvironment. Four groups were analyzed which contain Ctrl, CSF1R, IL10 and BF10. MTC-Q1 oral cancer cells were orthotopic injection in C57BL/6 mice. CD45-negatve cells has been isolated and RNA were extracted by Trizol, followed by cDNA were sequenced by Illumina NextSeq 550.

2023-07-09 | GSE193050 | GEO

Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity II

Project description:Bulk RNA sequence (RNA-seq) has been used to explore the effect of IL10/CSF1R fusion protein modulation in tumor microenvironment. Four groups were analyzed which contain Ctrl, CSF1R, IL10 and BF10. 4T1 breast cancer cells were orthotopic injection into Balb/c mice. tumor tissue has been isolated (~ 100 mm3) and total RNA were extracted by Trizol, followed by cDNA were sequenced by Illumina NextSeq 550.

2023-07-09 | GSE193045 | GEO

Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity V

2023-07-09 | GSE193054 | GEO

CSF1R-CAR T cells induce CSF1R signaling and promote target cell growth

Project description:Chimeric antigen receptor (CAR) T cells have revolutionized the landscape of cancer therapy, demonstrating unprecedented success in treating relapsed or refractory blood cancers. Previous studies of the mechanisms underlying the interactions and responses of CAR T cells and their targets have focused on the activation of CAR T cells and attempted to optimize CAR design to increase efficacy, while ignoring tumors and their responses to CAR ligation. We evaluated the signaling of a second-generation, ligand-based CAR built from the colony-stimulating factor 1 (CSF1) ligand to target the CSF1 receptor (CSF1R) on CSF1R-expressing target cells, and compared it to a conventional single-chain variable fragment (scFv)–based CAR against the B-cell antigen CD19 using stable isotope labeling by amino acids in cell culture (SILAC) co-culture with phosphotyrosine (pY) enrichment and liquid chromatography–tandem mass spectrometry (LC–MS/MS).. We showed that ligation of CSF1R-expressing THP-1 cells with CSF1R-CAR T cells stimulated CSF1R-like signaling in the THP-1 cells, whereas no target cell signaling response was observed after the ligation of CD19-CAR T cells with target Raji cells. In experiments with small-molecule inhibitors of the tyrosine kinase Lck, actin polymerization, and CSF1R, we found that CAR-induced CSF1R signaling in THP-1 cells depended exclusively on the kinase activity of CSF1R with no participation from T cell activation. Consistently, CSF1R-CAR T cells promoted THP-1 cell growth at low effector-to-target (E:T) ratios but prevented THP-1 cell growth at high E:T ratios. Our data provide evidence for an unintended consequence of CARs: CAR-induced signaling in cancer cells. These data may have broad implications for the choice of CAR antigen for optimal clinical efficacy.

2025-11-21 | PXD058576 | Pride

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