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STING agonists drive recruitment and intrinsic type I interferon responses in monocytic lineage cells for optimal anti-tumor immunity

ABSTRACT: STING agonists drive recruitment and intrinsic type I interferon responses in monocytic lineage cells for optimal anti-tumor immunity

PROVIDER: PRJNA1265750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33650100.fastq.gz	Fastqsanger.gz
	SRR33650101.fastq.gz	Fastqsanger.gz
	SRR33650102.fastq.gz	Fastqsanger.gz
	SRR33650103.fastq.gz	Fastqsanger.gz
	SRR33650104.fastq.gz	Fastqsanger.gz

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Similar Datasets

STING agonists drive recruitment and intrinsic type I interferon responses in monocytic lineage cells for optimal anti-tumor immunity

Project description:To define how intrinsic IFN-I signalling downstream of intratumoral STING agonist treatment alters the transcriptional state of myeloid cells, CITE-sequencing was performed on immune cells derived from the LNs and tumors of Ifnar1 mixed bone marrow chimeric mice treated with ADU-S100 or vehicle control.

2025-05-20 | GSE297709 | GEO

Context-dependent activation of STING-interferon signaling by CD11b agonists enhances anti-tumor immunity

Project description:Chronic activation of inflammatory pathways and suppressed interferon are hallmarks of immunosuppressive tumors. Previous studies have shown that CD11b integrin agonists could enhance anti-tumor immunity through myeloid reprograming, but the underlying mechanisms remain unclear. Herein we find that CD11b agonists alter tumor-associated macrophage (TAM) phenotypes by repressing NF-κB signaling and activating interferon gene expression simultaneously. Repression of NF-κB signaling involves degradation of p65 protein and is context independent. In contrast, CD11b agonism induces STING/STAT1 pathway-mediated interferon gene expression through FAK-mediated mitochondrial dysfunction, with the magnitude of induction dependent on the tumor microenvironment and amplified by cytotoxic therapies. Using tissues from phase I clinical studies, we demonstrate that GB1275 treatment activates STING and STAT1 signaling in TAMs in human tumors. These findings suggest potential mechanism-based therapeutic strategies for CD11b agonists and identify patient populations more likely to benefit.

2023-03-21 | GSE220959 | GEO

Intrinsic self-DNA triggers inflammatory disease dependent on STING (I)

Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type (WT), Trex1 deficient (TKO), STING deficient (SKO), or Trex1 and STING double deficient (STKO) mouse Heart

2014-07-09 | E-GEOD-59217 | biostudies-arrayexpress

RNASeq analysis of Myeloid Derived Suppressor Cells (MDSCs) from MC38 syngeneic mice to study their role on tumour intrinsic pathways (STING/IFN) for driving ceralasertib (AZD6738) efficacy

Project description:Understanding MoA of ceralasertib (AZD6738) in driving efficacy through immune regulation via polymorphonuclear-myeloid derived suppressor cells (PMN-MDSC) and monocytic-myeloid derived suppressor cells (M-MDSC) on tumour intrinsic pathways (STING/IFN) for AZD6738 driven efficacy. Animals were treated only for 7 days and left for further 7 days without treatment. We compared cells against Vehicle and spleen derived ( naive) as a positive control.

2024-01-30 | E-MTAB-13707 | biostudies-arrayexpress

Intrinsic self-DNA triggers inflammatory disease dependent on STING (II)

Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), Trex1 deficient MEFs (TKO) or STING and Trex1 double deficient MEFs (STKO) transfected with or without double strand DNA 90 (ISD) and examined cytokine production by these cells.

2014-07-09 | E-GEOD-59218 | biostudies-arrayexpress

Cascaded immunotherapy with implantable dual-drug depots sequentially releasing STING agonists and apoptosis inducers

Project description:Non-nucleotide stimulators of interferon gene (STING) agonists hold promise as immunotherapeutic agents for postsurgical adjuvant treatment of tumors. However, their limited effect duration hampers therapeutic effectiveness, necessitating prolonged administration of multiple doses that heightens infection risk and impacts patient compliance. Here, we develop an implantable dual-drug depot in a sandwich-like configuration, with a non-nucleotide STING agonist (MSA-2) in the outer layers of 3D-printed scaffolds and an immunogenic apoptosis inducer (doxorubicin, DOX) in the inner layer of electrospun fibers. We discover that MSA-2 can elicit endoplasmic reticulum stress-mediated and general immunogenic apoptosis of cancer cells. The stimulations with tumor-associated antigens and damage-associated molecular patterns from cancer cells, along with proinflammatory factors secreted by matured dendritic cells and M1-polarized macrophages, can depolymerize intracellular microtubules guiding activated STING trafficking towards lysosomes for degradation. Collectively, the dual-drug depots can initiate a long-lasting cascaded immunotherapy and chemotherapy, suppressing postsurgical tumor recurrence and metastasis.

2025-01-14 | GSE283208 | GEO

ExoSTING, an extracellular vesicle loaded with STING agonists, promotes tumor immune surveillance

Project description:Cyclic dinucleotide (CDN) agonists of the STimulator of InterferoN Genes (STING) pathway have shown immune activation and tumor clearance in pre-clinical models. However, CDNs administered intratumorally also promote STING activation leading to direct cytotoxicity of many cell types in the tumor microenvironment (TME), systemic inflammation due to rapid tumor extravasation of the CDN, and immune ablation in the TME. These result in a failure to establish immunological memory. ExoSTING, an engineered extracellular vesicle (EV) exogenously loaded with CDN, enhances the potency of CDN and preferentially activates antigen presenting cells in the TME. Following intratumoral injection, exoSTING was retained within the tumor, enhanced local Th1 responses and recruitment of CD8+ T cells, and generated systemic anti-tumor immunity to the tumor. ExoSTING at therapeutically active doses did not induce systemic inflammatory cytokines, resulting in an enhanced therapeutic window. ExoSTING is a novel, differentiated therapeutic candidate that leverages the natural biology of EVs to enhance the activity of CDNs.

2021-03-13 | GSE168784 | GEO

Microarray profiling of monocytic differentiaion reveals miRNA-mRNA intrinsic correlation

Project description:This SuperSeries is composed of the following subset Series: GSE26376: Microarray profiling of monocytic differentiaion reveals miRNA-mRNA intrinsic correlation (miRNA) GSE26377: Microarray profiling of monocytic differentiaion reveals miRNA-mRNA intrinsic correlation (gene expression) Refer to individual Series

2012-02-02 | E-GEOD-26379 | biostudies-arrayexpress

ExoSTING, an extracellular vesicle loaded with STING agonists, promotes tumor immune surveillance

Project description:ExoSTING, an extracellular vesicle loaded with STING agonists, promotes tumor immune surveillance

| PRJNA713983 | ENA

A Phosphotriester-Masked Dideoxy-cGAMP Derivative as a Cell-Permeable STING Agonist

Project description:2’3’-cyclic GMP-AMP (cGAMP) is a cyclic dinucleotide second messenger in which guanosine and adenosine are connected by one 3’-5’ and one 2’-5’ phosphodiester linkage. It is formed in the cytosol upon detection of pathogenic DNA by the enzyme guanosine-monophosphate-adenosine monophosphate synthase (cGAS). cGAMP subsequently binds to the adaptor protein stimulator of interferon genes (STING) to elicit an innate immune response leading to the production of type I interferons and cytokines. STING agonists are a highly promising avenue for an immuno-oncological anticancer therapy. A particular challenge with cyclic dinucleotide STING agonists are the two negative charges of the phosphodiester linkages, which strongly reduce the ability of such compounds to penetrate cell membranes. The development of cell-permeable STING agonists that can stimulate the immune system to enhance their anticancer potency is currently of utmost importance in the field. Here, we report the development of a dideoxy derivative of cGAMP as a phosphotriester prodrug, where the negative charge of the phosphate backbone has been masked with a thioester. We found that this thioester-protected compound features a dramatic increase in its cellular potency that rises from EC50 = 5 µM to 25 nM. The new compound is envisioned to enable an efficient STING-agonist-based anticancer therapy.

2025-05-07 | PXD057395 | Pride

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