Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effects of the C5aR1 blockade, Poly I:C and anti/PD1 combined treatment in the gene expression in LLC tumors

ABSTRACT: Effects of the C5aR1 blockade, Poly I:C and anti/PD1 combined treatment in the gene expression in LLC tumors

PROVIDER: PRJNA999384 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25443303_1.fastq.gz	Fastqsanger.gz
	SRR25443303_2.fastq.gz	Fastqsanger.gz
	SRR25443304_1.fastq.gz	Fastqsanger.gz
	SRR25443304_2.fastq.gz	Fastqsanger.gz
	SRR25443305_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Effects of the C5aR1 blockade, Poly I:C and anti/PD1 combined treatment in the gene expression in LLC tumors

Project description:In syngeneic solid tumor models, C5aR1 inhibition significantly enhanced the effectiveness of poly I:C, a toll-like receptor 3 (TLR3) agonist, combined with Programmed cell death protein 1 (PD-1)/Programmed cell death ligand-1 (PD-L1) blockade. In this experiment we aim to determine the effects of C5aR1 inhibition in the genes expression of Lewis Lung Cancer (LLC) tumors treated with poly I:C and PD-1 blockade combined treatment.

2024-11-20 | GSE239485 | GEO

miRNA expression between CD4+PD1+ and CD4+PD1- T cells

Project description:Recent success in cancer immunotherapy has come from the blockade of inhibitory receptors on T cells, such as programmed cell death-1, which can induce a state of T cell exhaustion upon constant antigen stimulation. Understanding miRNA regulation of PD1 can be useful to discover miRNAs for use in therapy or as prognostic markers in various diseases including cancer, autoimmunity and transplantation. We used microarrays to discover global miRNA expression changes upon PD1 upregulation and identified miRNAs that are both up- and down-regulated. B16F10 cells were injected subcutaneously into C57BL/6 mice and 16 days later CD4+PD1+ and CD4+PD1- were sorted from the lymph nodes and spleen for RNA extraction and hybridization on Affymetrix miRNA array.

2015-08-01 | E-GEOD-65208 | biostudies-arrayexpress

Blockade of C5aR1 resets M1 via gut microbiota-mediated PFKM stabilization in a TLR5-dependent manner

Project description:Increased researches show that complement, the codominant central mediator of humoral immunity, is a critical factor in tumor initiation, development, and chemotherapy resistance. C5a/C5aR1 signaling has been shown to promote tumor progression by recruiting MDSCs in breast malignancies And blockade of C5aR1 resets M1 via gut microbiota-mediated PFKM stabilization in a TLR5-dependent manner. We here report that TLR5 as a key regulator of tumor associated macrophages M1 polarization. Flagellin, the protein subunit of the bacterial flagellum, stimulates the innate immune receptor Toll-like receptor 5 (TLR5) after pattern recognition. Receptor activity was turned by a TLR5-flagellin interaction distal to the site of pattern recognition. Thus, activation of downstream signaling pathway is promoted.

2024-01-20 | GSE252048 | GEO

Gene expression profiling of mature dendritic cells from mice s. c. treated with GM-CSF-gene transduced LLC cells (LLC/SeV/GM) or control cells (LLC, LLC/SeV/GFP)

Project description:Irradiated granulocyte macrophage-colony stimulating factor (GM-CSF)-transduced autologous tumor cells induce substantial antitumor immunity through the maturation and migration of dendritic cells (DCs). However, little is known about the key molecules involved in GM-CSF-sensitized DCs (GM-DCs) in tumor draining lymph nodes (TDLNs). We initially confirmed that mice subcutaneously injected with poorly immunogenic syngeneic Lewis lung carcinoma (LLC) cells transduced with Sendai virus encoding GM-CSF (LLC/SeV/GM) significantly rejected the tumor growth. Using microarray expression profiling, we obtained a large number of gene expression data files from GM-DCs and control DCs in TDLNs, and subjected them to network-based cluster analysis and unexpectedly unraveled the expression levels of type I IFNs-related genes specifically expressed in plasmacytoid DCs (pDC) were robustly up-regulated in GM-DCs. In vivo depletion assay showed that pDC-depleted mice treated with subcutaneous LLC/SeV/GM cells abrogated the antitumor effects observed in control mice. Moreover combination use of imiquimod for TLR7 triggering on pDC with irradiated LLC/SeV/GM cells induced a significant therapeutic antitumor effect with marked induction of CD9+ pDC with antitumor phenotype, whereas other control mice groups had only minimal to-modest antitumor responses, implicating that this combined vaccine strategy using imiquimod could be promising for improvement of GM-CSF-induced antitumor immunity. Mouse GM-CSF induced gene expression in mature dendritic cells in tumor draining lymph nodes from C57/BL6N female mouse was measured at 2 days after s.c. tumor challenge with GM-CSF gene-transduced LLC cells (LLC/SeV/GM) or control cells (LLC, LLC/SeV/GFP).

2013-09-30 | E-GEOD-43169 | biostudies-arrayexpress

Single cell RNA sequence reveals C5aR1 inhibition selectively targets pro-tumorigenic M2 macrophages reversing PARP inhibitor resistance

Project description:Although Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi) have been approved in multiple diseases, including BRCA1/2 mutant breast cancer, responses are usually transient thus requiring the development of combination therapies that can capitalize on PARPi activity. We thus explored mechanisms underlying sensitivity and resistance to PARPi using two intrinsically sensitive and resistant syngeneic murine breast cancer models. Our data indicate that the PARPi sensitive tumor model has a high ratio of M1 anti-tumor/M2 pro-tumor macrophages with the M1/M2 ratio being increased by PARPi. In contrast the PARPi resistant tumor model had very low levels of M1 macrophages and thus a low M1/M2 ratio that was not altered by PARPi. Our data indicate that co-transplantation of the PARPi sensitive and the PARPi resistant tumor results in accumulation of M2 macrophages in the sensitive tumor, rendering the sensitive tumor PARPi resistant. C5aR1 and RPS19/C5aR1 signaling is selectively elevated in the M2 macrophages that are associated with PARPi resistance. Strikingly C5aR1 targeting decreased M2 macrophages, while sparing M1 macrophages rendering PARPi resistant tumors sensitive to PARPi. Consistent with the murine data, human breast cancers with high C5aR1 levels have a poor response to immune checkpoint blockade. Thus targeting C5aR1 may represent a therapeutic approach to selectively deplete M2 macropahges and engender sensitivity to PARPi and potentially other therapeutic approaches.

2023-06-30 | GSE215908 | GEO

Stop Mole LLC

Project description:Stop Mole LLC

| PRJNA1097484 | ENA

Combined blockade of CXCR4 and PD1 enhances intratumoral dendritic cell activation and immune responses against hepatocellular carcinoma

Project description:Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of unresectable hepatocellular carcinoma (HCC), but their impressive efficacy is seen in a fraction of patients. One key mechanism of immunotherapy resistance is the paucity of dendritic cells (DCs) in liver malignancies. Here, we tested the combined blockade of programmed death receptor 1 (PD1) and CXCR4, a receptor for CXCL12, a pleiotropic factor that mediates immunosuppression in tumors. Using orthotopic grafted and autochthonous HCC models with underlying liver damage, we evaluated treatment feasibility and efficacy.

2024-11-03 | GSE280861 | GEO

Transcription profiling of Mus musculus PBS vs IL-5 trerated LLC cells, and LLC vs B16 cells at baseline conditions

Project description:PBS and Il-5 (22 pM) treated LLC and B16 cells were harvested after 24 hours, for comparison between: 1) PBS and IL-5 trerated LLC cells, and 2) btween LLC and B16 cells at baseline conditions.

2010-12-13 | E-MEXP-2490 | biostudies-arrayexpress

Disruption of C5a/C5aR1 axis confers protection against hookworm infection in lung

Project description:Hookworms are soil-transmitted parasitic nematodes that penetrate the host skin before migrating to the lungs. With an estimated 500-700 million people infected worldwide, hookworm infections are a neglected tropical disease and a significant cause of morbidity, particularly in children, pregnant women, and immunocompromised individuals. Although there is ample evidence that complement activation is pivotal to elicit a protective host immune response against invasive pathogens, its role in hookworm infection remains insufficiently explored. Here, we investigated the complement anaphylatoxin, C5a, during the early lung stage of infection with Nippostrongylus brasiliensis in C57BL/6J wild type and C5aR1-/- mice. Despite the previously reported ability of lung larvae to evade complement activation, C5a was detectable locally in lung tissue and broncho-alveolar lavages. Surprisingly, C5aR1 presence directly contributed to the pathogenicity of hookworm infection. The burden of viable parasites in the lungs was mitigated in C5aR1-/- mice, compared to C57BL/6J mice 48 hours post-infection. Additionally, C5aR1-/- mice showed significantly reduced lung injury, lower cytokine release, attenuated alveolar hemorrhage, and limited alveolar-capillary barrier disruption. Neutrophils were the most abundant and highest C5aR1-expressing cell type in the alveolar space after infection. Deficiency of C5aR1 reduced the influx of neutrophils, monocytes, and eosinophils to the pulmonary airways. RNA sequencing of alveolar neutrophils revealed C5aR1-dependent regulation of the novel nuclear protein, DEDD2. In conclusion, our findings highlight the impact of C5aR1 signaling in neutrophils during hookworm infection uncovering an unexpected downside of complement activation in parasitic infection.

2024-08-29 | GSE272613 | GEO

Murine cells: MSC+LLC-serum-exosome vs LLC-serum-exosome

Project description:Murine cells: MSC+LLC-serum-exosome vs LLC-serum-exosome

| PRJNA490558 | ENA