Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cytokine-armored dendritic cell progenitors for antigen-agnostic cancer immunotherapy

ABSTRACT: Cytokine-armored dendritic cell progenitors for antigen-agnostic cancer immunotherapy

PROVIDER: PRJNA948418 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			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

Items per page:

1 - 5 of 34

Similar Datasets

Cytokine-armored dendritic cell progenitors for antigen-agnostic cancer immunotherapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-19 | GSE228164 | GEO

Tripartite target-agnostic combination immunotherapy cures established poorly immunogenic tumors

Project description:Single-agent immunotherapy, such as immune checkpoint inhibition, has shown remarkable efficacy in selected cancer entities and individual patients. However, most patients fail to respond. This is likely due to diverse immunosuppressive mechanisms acting in a concerted way to suppress the host anti-tumor immune response reducing the efficacy of single-agent immunotherapy. Combination immunotherapy approaches that are effective in such poorly immunogenic tumors mostly rely on precise knowledge of immunological targets on tumor cells by vaccinations or antibodies engineered to directly target those. Thus, creating a target-agnostic combination immunotherapy that is effective in poorly immunogenic tumors for which an immunological target is not known is a major challenge. We show that combined adoptive cellular therapy (ACT) with lymphokine-activated killer cells (LAKs), cytokine-induced killer cells (CIKs), Vγ9Vδ2-T-cells (γδ-T-cells) and adaptive, tumor-specific T-cells (CTLs) display synergistic anti-tumor treatment effects, which is further enhanced by co-treatment with anti-PD1 antibodies. Most strikingly, combination of this ACT with anti-PD1 antibodies, local immunotherapy of agonists against Toll-like receptor 3, 7 and 9 and pre-ACT lymphodepletion, a protocol we named TRI-IT, eradicates established, poorly immunogenic tumors and induces durable anti-tumor immunity in a variety of poorly immunogenic syngeneic, autochthonous, as well as autologous humanized patient-derived models. Mechanistically, we show that TRI-IT co-activates adaptive cellular and humoral, as well as innate anti-tumor immune responses to mediate its anti-tumor effect without inducing off-target toxicity. Our data demonstrate the efficacy of a target-agnostic combination immunotherapy that eradicates and potentially cures established poorly immunogenic tumors.

2022-10-28 | GSE173107 | GEO

NR2F6 deletion revives CAR‑T cell function and induces antigen‑agnostic immune memory in solid tumors

Project description:CAR‑T cell therapy is effective in hematologic malignancies but remains challenging in solid tumors owing to antigen heterogeneity and tumor microenvironment‑induced exhaustion. Here, gene editing of the nuclear receptor NR2F6 restores CAR‑T cell functionality, sustaining a TCF1⁺ progenitor‑exhausted T cell phenotype, enhancing metabolic fitness, and preserving cytotoxic potency under chronic antigen exposure. In immunocompetent models, Nr2f6‑deficient CAR‑T cells suppress solid tumor growth and induce robust, polyclonal host antitumor responses, as shown by protection in tumor re‑challenge experiments. Although infused CAR‑T cells disappear within 2 weeks, durable tumor control coincides with epitope spreading and secondary immune responses, likely via dendritic and other antigen‑presenting cell reactivation. Protection against antigen‑negative tumors and transferable immunity reveal a dual mode of direct cytotoxicity followed by durable immune reprogramming. This broadened host immunity may offset immune escape driven by antigen loss and tumor heterogeneity, establishing NR2F6 inhibition as a promising CAR‑T engineering strategy for durable, antigen‑agnostic solid‑tumor immunotherapy.

2026-01-23 | GSE284026 | GEO

Cytokine-armed dendritic cell progenitors for antigen-agnostic cancer immunotherapy.

Project description: Not available

| S-EPMC10899110 | biostudies-literature

Tripartite target-agnostic combination immunotherapy cures established poorly immunogenic tumors

Project description:Tripartite target-agnostic combination immunotherapy cures established poorly immunogenic tumors

| PRJNA723833 | ENA

IL-36γ Armored CAR T Cells Reprogram Neutrophils to Induce Endogenous Antitumor Immunity

Project description:Chimeric antigen receptor (CAR) T cells are ineffective against solid tumors due to obstacles of antigen heterogeneity and the immunosuppressive tumor microenvironment (TME). Previous efforts focused on enhancing cytotoxicity and persistence of CAR T cells, while the feasibility of improving their therapeutic efficacy by leveraging the modulatory effects of CAR T cells on host anti-tumor immunity remains unclear. Here, we report that IL-36γ armored CAR T cells eradicated primary solid tumors and enabled rejection of rechallenged antigen-negative tumors. IL-36γ armored CAR T cells favorably modulated the TME and reprogrammed unique neutrophil subsets with tumoricidal ability and antigen-(cross)presenting functions, resulting in the induction of endogenous T cells recognizing tumor antigens beyond CAR-targeted antigens. Our study demonstrates that neutrophil engagement by CAR T cells is a critical step in the establishment of the cancer-immunity cycle and introduces a broadly applicable method to overcome key barriers to adoptive cell therapies for solid tumors.

2026-03-01 | GSE307110 | GEO

IL-36γ Armored CAR T Cells Reprogram Neutrophils to Induce Endogenous Antitumor Immunity

2026-03-27 | GSE307092 | GEO

IL-36γ Armored CAR T Cells Reprogram Neutrophils to Induce Endogenous Antitumor Immunity

2025-12-31 | GSE306905 | GEO

Gene expression from armored CAR T cell

Project description:Compare the gene expression profile among armored IL-18 secreting CAR T cells and second-generation CAR T cells

2017-04-03 | GSE97343 | GEO

Gene expression from armored CAR T cell and TAMs

Project description:Compare the gene expression profile among armored IL-12 secreting CAR T cells and second-generation CAR T cells and TAMs recovered from both groups

2017-07-24 | GSE97665 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data