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Effect of Flt3L and DNGR-1 on the biology of tumor-infiltrating type 1 dendritic cells

ABSTRACT: Effect of Flt3L and DNGR-1 on the biology of tumor-infiltrating type 1 dendritic cells

PROVIDER: PRJNA607519 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11112561.fastq.gz	Fastqsanger.gz
	SRR11112562.fastq.gz	Fastqsanger.gz
	SRR11112563.fastq.gz	Fastqsanger.gz
	SRR11112564.fastq.gz	Fastqsanger.gz
	SRR11112565.fastq.gz	Fastqsanger.gz

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Effect of Flt3L and DNGR-1 on the biology of tumor-infiltrating type 1 dendritic cells

Project description:DNGR-1 is a dead cell-sensing receptor specifically expressed in type 1 conventional dendritic cells (cDC1s), but whether it plays a role in antitumor immunity remains unexplored. In our work we have explored the transcriptional profile of tumor-infiltrating cDC1s competent or deficient in DNGR-1,

2021-05-19 | GSE145534 | GEO

Expression data from Flt3L-derived bone marrow dendritic cells from WT or Clec9agfp/gfp mice treated or not with dead cells

Project description:DNGR-1 (CLEC9A) is expressed in CD8-like dendritic cells (DCs) and detects a ligand exposed on necrotic cells. We have characterized the transcripts that are induced in cultures of Flt3L-derived bone-marrow-derived WT or DNGR1-deficient DCs upon incubation with dead cells. Microarray analysis of the transcriptome of DNGR-1-deficient and WT DCs cultured with dead cells failed to reveal any DNGR-1-dependence in the transcriptional response to dead cells. Flt3L-BMDC from WT or DNGR-1-deficient (Clec9a gfp/gfp) mice were left untreated or were cultured for 5 hours with UV-treated dead cells at a 1:2 ratio. CD24hi CD11blow B220- CD8Î±+-like DC were purified by cell sorting and RNA was extracted. There were 3 replicates for each of the four experimental conditions.

2012-04-30 | E-GEOD-36435 | biostudies-arrayexpress

Expression data from Flt3L-derived bone marrow dendritic cells from WT or Clec9agfp/gfp mice treated or not with dead cells

2012-05-01 | GSE36435 | 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

Gene expression profile of MHCII+ cell subsets from bone marrow culture with FLT3L or GM-CSF

Project description:BM culture comprises of various cell types including dendritic cells and macrophage-like cells. To understand the biology of BM-derived DCs, CD11c+MHCII+ cell subsets from BM cultures with FLT3L or GM-CSF were analyzed and are shown to have distinct transcriptional profiles.

2023-03-05 | GSE225321 | GEO

Gene expression dynamics of Flt3L induced ex vivo BMDC differentiation

Project description:To understand the gene expression dynamics during Flt3L induced Bone-marrow derived dendritic cell (BMDC) differentatiion we performed RNA-seq. Three distinct stages were chosen and included the initial bone marrow cells, the Common Myeloid Progenitor (CMP), and fully differentiated BMDC.

2023-11-06 | GSE107026 | GEO

DNA methylation dynamics of Flt3L induced ex vivo BMDC differentiation

Project description:To understand the DNA methylation dynamics during Flt3L induced Bone-marrow derived dendritic cell (BMDC) differentatiion we performed reduced representation bisulfite sequencing (RRBS). Three distinct stages were chosen and included the initial bone marrow cells, the Common Myeloid Progenitor (CMP), and fully differentiated BMDC.

2023-11-06 | GSE107027 | GEO

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

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

| PRJNA622704 | ENA

The Flt3L/Flt3 Axis in Dendritic Cell Biology and Cancer Immunotherapy.

Project description:Dendritic cells (DCs) prime anti-tumor T cell responses in tumor-draining lymph nodes and can restimulate T effector responses in the tumor site. Thus, in addition to unleashing T cell effector activity, current immunotherapies should be directed to boost DC function. Herein, we review the potential function of Flt3L as a tool for cancer immunotherapy. Flt3L is a growth factor that acts in Flt3-expressing multipotent progenitors and common lymphoid progenitors. Despite the broad expression of Flt3 in the hematopoietic progenitors, the main effect of the Flt3/Flt3L axis, revealed by the characterization of mice deficient in these genes, is the generation of conventional DCs (cDCs) and plasmacytoid DCs (pDCs). However, Flt3 signaling through PI3K and mTOR may also affect the function of mature DCs. We recapitulate the use of Flt3L in preclinical studies either as a single agent or in combination with other cancer therapies. We also analyze the use of Flt3L in clinical trials. The strong correlation between type 1 cDC (cDC1) infiltration of human cancers with overall survival in many cancer types suggests the potential use of Flt3L to boost expansion of this DC subset. However, this may need the combination of Flt3L with other immunomodulatory agents to boost cancer immunotherapy.

| S-EPMC8037622 | biostudies-literature

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

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