Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome profiling of lymph nodes from Spink5 conditional knock-out mice.

ABSTRACT: We generated a viable mouse model of Netherton syndrome by conditional ablation of Spink5 gene in the epidermis. To study the systemic inflammation phenotype of this mouse model at the molecular level, we induced Spink5 deletion in the skin of young adult mice and collected inguinal lymph nodes for transcriptome analyses.

ORGANISM(S): Mus musculus

PROVIDER: GSE224409 | GEO | 2024/02/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome profiling of lesional skin from Spink5 conditional knock-out mice

Project description:We generated a viable mouse model of Netherton syndrome by conditional ablation of Spink5 gene in the epidermis. To characterize this model at the molecular level, we induced Spink5 deletion in young adult mice and collected lesional skin samples for transcriptome analyses.

2024-02-05 | GSE224280 | GEO

Comparative analyses of Netherton syndrome patients and Spink5 conditional knock-out mice define disease-relevant pathways

Project description:Netherton syndrome (NS) is a rare skin disease caused by loss-of-function mutations in the serine peptidase inhibitor Kazal type 5 (SPINK5) gene. Disease severity and the lack of efficacious treatments call for a better understanding of NS mechanisms. Here we describe a viable, Spink5 conditional knock-out (cKO) mouse model, allowing to study NS progression. Using comparative transcriptomics and proteomics, we determine a disease molecular profile conserved in mouse models and NS patients. Spink5 cKO mice and NS patients share skin barrier and inflammation signatures defined by up-regulation of proteases, IL-17, IL-36, IL-20 family cytokines. Furthermore, we show that systemic inflammation in Spink5 cKO mice is associated with thymic atrophy and is driven by innate immunity and IL-17/IL-22 signaling. By comparing skin transcriptomes and proteomes, we uncovered several putative substrates of tissue kallikrein-related proteases (KLKs), demonstrating that KLKs can proteolytically regulate IL-36 pro-inflammatory cytokines. Our study thus provides a conserved molecular framework for NS disease, adding new insights into its mechanisms and therapeutic targets.

2023-02-02 | MSV000091184 | MassIVE

Transcriptome profiling of lesional skin from neonate Spink5 constitutive knock-out mice

Project description:Spink5 constitituve knock-out mice mimic the disease features of Netherton syndrome but die within several hours after birth due to severe skin barrier defect. To characterize the skin barrier and skin inflammation phenotype of this mouse model at the molecular level, we collected back skin samples from mice shortly after their birth.

2024-02-05 | GSE224674 | GEO

Transcriptome profiling of lesional skin from 3-week-old Tg.hKLK5 mice

Project description:Transgenic mice over-experssing human KLK5 (Tg.hKLK5) in the epidermis develop an inflammatory skin phenotype resembling Netherton syndrome. To characterize the skin inflammation phenotype of this mouse model at the molecular level, we collected back skin samples from young mice at three weeks of age, when the skin phenotype is most severe.

2024-02-05 | GSE224673 | GEO

Expression data from classical dendritic cells isolated from mouse lymph nodes

Project description:Dendritic cells increase expression of pro-inflammatory cytokines and chemokines and undergo metabolic reprogramming upon TLR activation. Mice fed conventional diet (CD) or 60% high-fat diet (HFD) were treated by skin application of imiquimod (IMQ) during 6 days and classical dendritic cells (cDC) were isolated from inguinal lymph nodes (iLN) to reveal inflammatory and metabolic pathways that are sensitive to TLR7/8 activation and a high fatty acid environment. We used microarray to identify pathways in classical dendritic cells from IMQ-treated mice that link inflammation and metabolism in a high fatty acid environment.

2019-06-30 | GSE110963 | GEO

Single cell immune response to the mRNA SARS-CoV-2 vaccine and yellow fever in the lymph nodes of mice

Project description:Purpose: to understand the mechanisms of vaccines in the lymph nodes of mice Methods: mice were treated with mRNA SARS-CoV-2 vaccine or the yellow fever vaccine. The draining inguinal or illiac lymph nodes were harvested 1, 3, or 7 days after treatment and analyzed by scRNA-seq Results: TBD Conclusions: TBD

2022-01-30 | GSE179131 | GEO

Transcription Profiles of Regulatory T Cells in Follicular Lymphoma Lymph Nodes, Normal Lymph Nodes and Reactive Lymph Nodes

Project description:We have previously shown that Tregs infiltrating follicular lymphoma lymph nodes (FLN) are quantitatively and qualitatively different than those infiltrating normal and reactive nodes (NLN, RLN, respectively). To gain insight into how such Treg populations differ, we performed RNA sequence (RNAseq) analyses on flow sorted Tregs from all three sources. We identify several molecules that could contribute to the observed increased suppressive capacity of FLN tregs, including upregulation of CTLA-4, IL-10, and GITR, all confirmed by protein expression. In addition, we identify, and confirm functionally, a novel mechanism by which Tregs target to and accumulate within a human tumor microenvironment, through the down regulation of S1PR1, SELL (L-selectin) and CCR7, potentially resulting in greater lymph node retention. In addition we identify and confirm functionally the upregulation of CXCR5, CXCL13 and IL-16 demonstrating the unique ability of the follicular derived Tregs to localize and accumulate within not only the malignant lymph node, but also localize and accumulate within the malignant B cell follicle itself. Such findings offer significant new insights into how FLN Tregs may contribute to the biology of follicular lymphoma and identify several novel therapeutic targets.

2016-05-26 | GSE74102 | GEO

Expression of marker genes in the lymph nodes predicts the recurrence of squamous cell vulvar carcinoma.

Project description:BACKGROUND: Regional lymph node (LN) status is a well-known prognostic factor for vulvar carcinoma (VC) patients. Although the reliable LN assessment in VC is crucial, it presents significant diagnostic problems. PURPOSE: We aimed to identify specific mRNA markers of VC dissemination in the LN and to address the feasibility of predicting the risk of nodal recurrence by the patterns of gene expression. EXPERIMENTAL DESIGN: Sentinel and inguinal LN samples from 20 patients who had undergone surgery for stage T1-3, N0-2, M0 primary vulvar squamous cell carcinoma were analyzed. Gene expression profiles were assessed in four metastatic [LN(+)] and four histologically negative [LN(-)] lymph node samples obtained from four VC patients, by the Affymetrix U133 Plus 2.0 gene expression microarrays. Of the set of genes of the highest expression in the metastatic LNs compared to LN(-), seven candidate marker genes were selected PERP, S100A8, FABP5, SFN, CA12, JUP and CSTA, and the expression levels of these genes were further analyzed by the real-time reverse transcription polymerase chain reaction (qRT-PCR) in 71 LN samples. RESULTS: Five of the genes, PERP, S100A8, FABP5, SFN and CA12, were significantly increased in LN(+) compared to LN(-) samples. In the initial validation of the seven putative markers of metastatic LN, the Cox proportional hazard model pointed to SFN and CA12 expression to significantly relate to the time to groin recurrence in VC patients. CONCLUSIONS: PERP, S100A8, FABP5, SFN and CA12 have a potential of marker genes for the molecular testing of LN involvement in VC patients. Gene expression profiles of 8 tissue samples representing 4 metastatic [N(+)] and 4 histologically negative [N(-)] LN samples

2011-07-31 | E-GEOD-28442 | biostudies-arrayexpress