Dataset Information

Proteomics of preclinical model of skin dermatitis

ABSTRACT: To assess the preclinical Aldara model, the proteomic response of mouse skin to topical applied Aldara cream was assessed using untargeted LC-MS. Skin from sham treated or treated with the Aldara cream were compared for 4 independent experiments after 8 days of treatment.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Skin

SUBMITTER: Peter Blattmann

LAB HEAD: Peter Blattmann

PROVIDER: PXD056245 | Pride | 2025-04-22

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20240920_145749_ELB0427-0114_mouse_Report.tsv	Tabular
	240920_SP_Mouse.fasta	Fasta
	ELB0427-0024_sample1.raw	Raw
	ELB0427-0024_sample10.raw	Raw
	ELB0427-0024_sample11.raw	Raw

Items per page:

1 - 5 of 64

Publications

Efficacy of IDOR-1117-2520, a novel, orally available CCR6 antagonist in preclinical models of skin dermatitis.

Kulig Paulina P Brazauskas Pijus P Suffiotti Madeleine M Raoult Emilie E Babilonski Ulrike U Renault Bérengère B Grieder Ursula U Vezzali Enrico E Blattmann Peter P Martinic Marianne M MM Murphy Mark J MJ

British journal of pharmacology 20250328

<h4>Background and purpose</h4>The chemokine receptor CCR6 guides pathogenic T17 cells, implicated in autoimmune diseases including psoriasis, to sites of inflammation via the chemokine CCL20. Therefor, pharmacological inhibition of CCR6<sup>+</sup> immune cell migration provides a novel therapeutic approach. Translatability of such an intervention has not yet been assessed in detail. We evaluated the translatability of the Aldara® mouse model induced skin inflammation to psoriasis, with particu ...[more]

PMID: 40156059

Similar Datasets

Project description:Genes involved in the inflammatory response resulting in allergic contact dermatitis (ACD) are only partly known. In this study, we introduce the use of high density oligonucleotide arrays for gene expression profiling in human skin during the elicitation of ACD. Skin biopsies from normal and nickel-exposed skin were obtained from 7 nickel-allergic patients and 5 non-allergic controls at four different time points during elicitation of eczema: 0h, 7h, 48h and 96h. Each gene expression profile was analysed by hybridization to high density oligonucletide arrays. Cluster analysis of 74 genes found to be differentially expressed in the patients over time revealed that the patient samples may be categorised into two groups: An early time point group (0h and 7h) and a late time point group (48h and 96h). Compared to the early time points, late time point skin samples were characterised by the up-regulation of inflammatory molecules including genes involved in the class I antigen presenting pathway and genes involved in lymphocyte adhesion and motility ; Correspondence analysis including both patients and controls revealed three distinct groups: i) the control group, ii) the early time point patient group (0h and 7h) and iii) the late time point patient group (48h and 96h). Experiment Overall Design: For the microarray study, 7 nickel-allergic patients and 5 non-allergic controls were recruited. All subjects were female. The skin covering the upper nates was exposed to nickel delivered during a patch test. Skin biopsies were taken to generate a time-series. Skin was exposed to nickel for 0h, 7h, 48h and 96h. Experiment Overall Design: All nickel allergic patients reacted with visible eczama at the 48h and 96h time-points. No eczema was vissible at the 0h or 7h time-points. Control subjects did not show visible eczema at any time-point. Experiment Overall Design: RNA was extracted from the skin biopsies and 34 biopsies yielded RNA of sufficient quantity and quality for micro-array analysis.