Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cancer-Associated Fibroblast Secreted Collagen is associated with Immune Suppressive LAIR-1 in Gliomas

ABSTRACT: Cancer-Associated Fibroblast Secreted Collagen is associated with Immune Suppressive LAIR-1 in Gliomas

PROVIDER: PRJNA1048387 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27042800.fastq.gz	Fastqsanger.gz
	SRR27042801.fastq.gz	Fastqsanger.gz
	SRR27042802.fastq.gz	Fastqsanger.gz
	SRR27042803.fastq.gz	Fastqsanger.gz
	SRR27042804.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 40

Similar Datasets

Cancer-Associated Fibroblast Secreted Collagen is associated with Immune Suppressive LAIR-1 in Gliomas

Project description:This is for a research letter in which we use peds glioma data to show collagen expression and CAFs are more abundant in the high grade glioma over low grade gliomas and additionally report the presence of LAIR1 in close proximity with these collagen rich areas.

2023-12-09 | GSE249263 | GEO

The effect of LAIR-1 ligation on naïve CD8 T cells

Project description:To assess the role of LAIR-1 signalling on CD3 stimulated CD8 T cells, we ligated LAIR-1 on CD8 T cells during CD3 mediated CD8 T cell stimulation

2024-01-24 | GSE228709 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the implication of LAIR-1 in sorted mouse pulmonary ILC2 Transcriptomes

Project description:Type-2 innate lymphoid cells (ILC2s) are central players in type-2 asthma. They initiate eosinophil infiltration and airway hyperreactivity (AHR) through cytokine secretion. Leukocyte-associated immunoglobulin-like receptor 1 (LAIR-1) is an inhibitory receptor considered as immune checkpoint in different inflammatory diseases. Here we assessed the role of LAIR-1 in murine ILC2s. WT and LAIR-1 KO mice were intranasally challenged with IL-33 and pulmonary ILC2s were sorted to perform RNA sequencing. Our results unravel a novel regulatory axis in ILC2s with the capacity to reduce their activation.

2021-04-10 | GSE171819 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the implication of LAIR-1 in sorted lung macrophage Transcriptomes

Project description:Recent studies reported the inhibitory properties of LAIR-1 in different inflammatory diseases, including allergic and viral airway inflammation. However, the implication of LAIR-1 in ALI/ARDS remains unknown. Poly(I:C), a synthetic analog of (ds)RNA was administrated intranasally to mimic acute inflammation in viral infections and therefore induce experimental ALI/ARDS. RNA sequencing approach was used to explore and compare lung macrophage transcriptomic profiles in wild-type and LAIR-1 knock-out mice.

2023-09-01 | GSE216259 | GEO

Remodeling of the tumor microenvironment via blockade of LAIR-1 and TGF-β signaling [bulk RNA-seq]

Project description:Collagens in the extracellular matrix (ECM) provide a physical barrier to tumor immune infiltration, while also acting as a ligand for immune inhibitory receptors. Transforming growth factor-β (TGF-β) is a key contributor to shaping the ECM by stimulating the production and remodeling of collagens. TGF-β-activation signatures and collagen-rich environments have both been associated with T-cell exclusion and lack of responses to immunotherapy. Here we describe the effect of targeting collagens that signal through the LAIR-1 inhibitory receptor in combination with blockade of TGF-β and programmed cell death ligand 1 (PD-L1). This approach remodeled the tumor collagenous matrix, enhanced tumor infiltration and activation of CD8+ T cells, and repolarized suppressive macrophage populations resulting in high cure rates and long-term tumor-specific protection across murine models of colon and mammary carcinoma. The results highlight the advantage of direct targeting of ECM components in combination with immune checkpoint blockade therapy.

2022-03-09 | GSE195685 | GEO

Remodeling of the tumor microenvironment via blockade of LAIR-1 and TGF-β signaling [single cell RNA-seq]

2022-03-09 | GSE194421 | GEO

Tumor-associated macrophages derived from circulating inflammatory monocytes degrade collagen through cellular uptake

Project description:Physiologic turnover of interstitial collagen is mediated by a sequential pathway, in which collagen is fragmented by pericellular collagenases, endocytosed by specific collagen receptors, and routed to lysosomes for degradation by lysosomal cathepsins. Here, we used intravital microscopy to investigate if malignant tumors, which are characterized by high rates of extracellular matrix turnover, utilize a similar collagen degradation pathway. Tumors of epithelial, mesenchymal, or neural crest origin all displayed vigorous endocytic collagen degradation with an abundance of cells engaged in this process. These cells were identified as tumor-associated macrophage (TAM)-like cells that degraded collagen in a mannose receptor-dependent manner. Accordingly, increased intra-tumoral collagen was observed in mannose receptor-deficient mice. Whole transcriptome profiling uncovered a distinct extracellular matrix-catabolic signature of these collagen-degrading TAMs. Lineage-ablation studies revealed that collagen-degrading TAMs originated from circulating CCR2+ monocytes. The study identifies a novel function of TAMs in altering the tumor microenvironment through endocytic collagen turnover and establishes macrophages as centrally engaged in tumor-associated collagen degradation.

2018-01-01 | GSE107053 | GEO

Cancer immunotherapy by NC410, a LAIR-2 Fc protein blocking human LAIR-collagen interaction.

Project description:Collagens are a primary component of the extracellular matrix and are functional ligands for the inhibitory immune receptor leukocyte-associated immunoglobulin-like receptor (LAIR)-1. LAIR-2 is a secreted protein that can act as a decoy receptor by binding collagen with higher affinity than LAIR-1. We propose that collagens promote immune evasion by interacting with LAIR-1 expressed on immune cells, and that LAIR-2 releases LAIR-1-mediated immune suppression. Analysis of public human datasets shows that collagens, LAIR-1 and LAIR-2 have unique and overlapping associations with survival in certain tumors. We designed a dimeric LAIR-2 with a functional IgG1 Fc tail, NC410, and showed that NC410 increases human T cell expansion and effector function in vivo in a mouse xenogeneic-graft versus-host disease model. In humanized mouse tumor models, NC410 reduces tumor growth that is dependent on T cells. Immunohistochemical analysis of human tumors shows that NC410 binds to collagen-rich areas where LAIR-1+ immune cells are localized. Our findings show that NC410 might be a novel strategy for cancer immunotherapy for immune-excluded tumors.

| S-EPMC8225389 | biostudies-literature

Pembrolizumab in Treating Younger Patients With Recurrent, Progressive, or Refractory High-Grade Gliomas, Diffuse Intrinsic Pontine Gliomas, Hypermutated Brain Tumors, Ependymoma or Medulloblastoma

Project description:This phase I trial studies the side effects and best dose of pembrolizumab and to see how well it works in treating younger patients with high-grade gliomas (brain tumors that are generally expected to be fast growing and aggressive), diffuse intrinsic pontine gliomas (brain stem tumors), brain tumors with a high number of genetic mutations, ependymoma or medulloblastoma that have come back (recurrent), progressed, or have not responded to previous treatment (refractory). Immunotherapy with monoclonal antibodies, such as pembrolizumab, may induce changes in the body’s immune system, and may interfere with the ability of tumor cells to grow and spread.

| 2183538 | ecrin-mdr-crc

Enhanced Collagen Secretion in Epithelial Cancer Cells is associated with L1CAM Deficiency

Project description:Collagen, a critical component of the tumor microenvironment (TME), significantly influences cancer-associated fibrosis, tissue stiffness, immune response, and metastasis. Pancreatic ductal adenocarcinoma (PDAC) is characterized by excessive collagen deposition, and effective therapies remain limited. Our research challenges conventional understanding by highlighting the remarkable ability of specific tumor epithelial populations, particularly those with low levels of L1 cell adhesion molecule (L1CAM) expression (L1low), to actively modulate collagen dynamics within the TME. Transcriptome analysis of PDAC cells with varying L1 expression reveals shifts in collagen-related pathways, with heightened expression of collagen 17A1 (COL17A1) in L1low cells. Alongside, L1low cells exhibit enhanced migratory capacity. In an orthotopic mouse model, L1low cancer cells demonstrate increased collagen deposition, resistance to gemcitabine treatment, and an elevated propensity for liver metastases. Treatment with Tranilast, an anti-fibrotic drug, significantly reduces tumor volume and collagen deposition while enhancing L1 expression. This, in turn, mitigates tumor invasiveness and suppresses metastases formation. Overall, our study uncovers a novel role for L1CAM in PDAC aggressiveness and fibrosis, revealing a new epithelial population capable of collagen secretion and challenging the traditional notion that this function is solely attributed to stromal cells.

2024-06-11 | GSE268948 | 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