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TCR profiling of whole MC38 tumors, treated with PBS + IgG , Cis + PBS + aPD-1, Cis + DCP-IL-12/FLT3L + IgG or Cis + DCP-IL-12/FLT3L + ɑPD-1.

ABSTRACT: TCR profiling of whole MC38 tumors, treated with PBS + IgG , Cis + PBS + aPD-1, Cis + DCP-IL-12/FLT3L + IgG or Cis + DCP-IL-12/FLT3L + ɑPD-1.

PROVIDER: PRJNA948415 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23958146.fastq.gz	Fastqsanger.gz
	SRR23958147.fastq.gz	Fastqsanger.gz
	SRR23958148.fastq.gz	Fastqsanger.gz
	SRR23958149.fastq.gz	Fastqsanger.gz
	SRR23958150.fastq.gz	Fastqsanger.gz

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TCR profiling of whole MC38 tumors, treated with PBS + IgG , Cis + PBS + aPD-1, Cis + DCP-IL-12/FLT3L + IgG or Cis + DCP-IL-12/FLT3L + ɑPD-1.

Project description:Dendritic cells (DCs) are specialized myeloid cells with the ability to uptake, process, and present antigens to T lymphocytes. They also generate cytokine and chemokine gradients that regulate immune cell trafficking, activation, and function. Monocyte-derived DCs (moDCs) pulsed with tumor antigens have been used as a platform for therapeutic vaccination in cancer. However, in spite of significant development and testing, antigen-loaded moDCs have delivered mixed clinical results. Here we present a DC therapy that uses a population of mouse or human DC progenitors (DCPs) engineered to produce two immunostimulatory cytokines, IL-12 and FLT3L. In the absence of antigen loading, cytokine-armored DCPs efficiently differentiated into conventional type I DCs (cDC1) and inhibited tumor growth in melanoma and autochthonous liver cancer models. Tumor response to DCP therapy involved synergy between IL-12 and FLT3L and was associated with early NK cell activation and massive effector T cell infiltration, robust M1-like macrophage programming, and ischemic tumor necrosis. Mechanistically, anti-tumor immunity was dependent on endogenous cDC1 expansion and interferon-γ (IFNγ) production and signaling, but did not require CD8+ T cell cytotoxicity. In one application, cytokine-armored DCPs synergized with antigen-specific CAR-T cells to eradicate intracranial gliomas in mice.

2023-09-19 | GSE228161 | GEO

Single cell expression profiling of whole B16F10 melanoma tumors, treated with PBS or DCP-IL-12/FLT3L.

2023-09-19 | GSE228014 | GEO

Single cell expression profiling of whole B16F10 melanoma tumors, treated with PBS or DCP-IL-12/FLT3L.

Project description:Single cell expression profiling of whole B16F10 melanoma tumors, treated with PBS or DCP-IL-12/FLT3L.

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Staphylococcus aureus strain:DCP

Project description:Staphylococcus aureus strain:DCP Genome sequencing

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Stutzerimonas stutzeri strain:DCP-Ps1

Project description:Stutzerimonas stutzeri strain:DCP-Ps1 Genome sequencing and assembly

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Flt3L in Treating Patients With Metastatic Colorectal Cancer

Project description:RATIONALE: Flt3L may stimulate a person’s immune system and help kill tumor cells. PURPOSE: Phase I trial to study the effectiveness of flt3L given to patients before undergoing surgery to remove metastases from colorectal cancer.

| 2002961 | ecrin-mdr-crc

Comparison between CD103+ cDC1s from IL-33-treated Flt3L-BMDCs and GM-CSF-treated Flt3L-BMDCs

Project description:To assess genotypic differences between IL-33-induced CD103+ cDC1s and GM-CSF-induced CD103+ cDC1s IL-33 or GM-CSF was treated at 5 ng/ml on the day 5 of Flt3L-BMDC generation and then the cells were incubated for an additional 5 days Then, we performed RNA sequencing of CD103+ cDC1s isolated from IL-33 or GM-CSF-treated Flt3L-BMDCs

2023-05-30 | GSE226585 | GEO

Transcription profiling of wild type and Pdr1 and Pdr3 knock-out yeast treated with detergents DCP (2-4-dichlorophenol) and POELE (polyoxyethylen-9-laurylether)

Project description:DCP (2-4-dichlorophenol; 0,3mM) and POELE (polyoxyethylen-9-laurylether; 0,1mM)treatment on Saccharomyces cerevisiae W303-1A wild-type cells. Further investigation of the involvement of the transcripton factors Pdr1 and Pdr3 in DCP treated cells. Cells were growing in early exponential phase in rich medium.

2007-10-09 | E-MEXP-865 | biostudies-arrayexpress

Flt3L therapy induces a Treg‐promoting cDC1 state in triple‐negative breast cancer

Project description:Conventional dendritic cells (cDCs) are at the forefront of activating the immune system to mount an anti‐tumor immune response. Flt3L is a cytokine required for DC development that can increase DC abundance in the tumor when administered therapeutically. However, the impact of Flt3L on the phenotype of distinct cDC subsets in the tumor microenvironment is still largely undetermined. Here, using multi‐omic single‐cell analysis, we show that Flt3L therapy increases all cDC subsets in orthotopic E0771 triple‐negative breast cancer, but this did not result in a reduction of tumor growth. Interestingly, a CD81+migcDC1 population, likely developing from cDC1, was induced upon Flt3L treatment. This subset is characterized by the expression of both canonical cDC1 markers as well as migratory cDC activation and regulatory markers and displayed a higher Treg‐inducing potential compared to other migcDCs. To shift the cDC phenotype towards a T‐cell stimulatory phenotype, CD40 agonist therapy was administered in combination with Flt3L. However, while αCD40 reduced tumor growth, Flt3L failed to improve the therapeutic response to αCD40 therapy. Interestingly, Flt3L+αCD40 combination therapy increased the abundance of Treg promoting CD81+migcDC1. Nonetheless, while Treg‐depletion and αCD40 therapy were synergistic, the addition of Flt3L to this combination did not result in any added benefit. Overall, these results indicate that merely increasing cDCs in the tumor by Flt3L treatment cannot improve anti‐tumor responses and therefore might not be beneficial for the treatment of triple‐negative breast cancer, though could still be of use to increase cDC numbers for autologous DC‐therapy.

2023-07-26 | GSE225539 | GEO

The clonal and molecular aetiology of Flt3L-mediated ‘emergency’ dendritic cell development

Project description:Flt3 ligand (Flt3L) promotes an increased generation of type 1 conventional dendritic cells (cDC1s), resulting in enhanced immunity against infections and cancer. Here, we employ cellular barcoding to understand how Flt3L regulates single haematopoietic stem and progenitor cell (HSPC) fate. Our results demonstrate that although Flt3L stimulation can recruit some additional cDC1-generating HSPCs, the major contributing factor to higher cDC1 numbers is through enhanced clonal expansion. This selective cDC1 expansion occurs primarily via multi-/oligo-potent clones, without compromising their clonal output to other lineages. We then develop Divi-Seq to simultaneously profile division history, surface phenotype and the transcriptional state of single HSPCs during the early phase of the response. We discover that Flt3L-responsive HSPCs maintain a proliferative ‘early progenitor’-like state, which leads to a selective emergence of CD11c+cKit+ transitional precursors with high cellular output to cDC1s. These findings inform the mechanistic action of Flt3L in natural immunity and immunotherapy.

2020-04-03 | GSE147977 | GEO

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