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Single cell analysis of epidermis from nickel-challenged skin

ABSTRACT: In this study, we investigated the consequences of repetitive nickel challenge at previously nickel-challenged skin sites in allergic participants. Repeated challenge with nickel resulted in progressive worsening allergic skin reactions in nearly all participants (11 out of 12). To investigate the immunopathogenesis of nickel in allergic contact dermatitis (ACD), clinically cleared epidermal skin taken 21 days after each challenge was analyzed by immunohistochemistry, flow cytometry and single-cell RNA sequencing (scRNA-seq). Correlating with the worsening skin reactions, an expanding pool of epidermal CD4+ and CD8+ tissue-resident memory T (TRM) cells was seen locally in the challenged skin. Using scRNA-seq a broad subset of TRM cells with various effector phenotypes was identified, which included a predominant population of type 2 T helper (TH2) and KIR+CD8+ TRM cells that expanded with repeated challenge. We observed, broad clonal expansion after nickel challenge with interindividual variations, and clonally related clusters of less differentiated cells which may supply more developed effector TRM cells. Furthermore, repetitive challenge resulted in an increasing population of exhausted regulatory T (Treg) cells that showed lesser clonal expansion. Collectively, our data suggests that repeated challenge to nickel leads to aggravation of eczema and is supported by the increased numbers of effector TRM cells, phenotype differentiation, clonal expansion, and exhaustion of Treg cells in the challenged skin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE246179 | GEO | 2025/11/09

REPOSITORIES: GEO

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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.

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Single cell analysis of epidermis from nickel-challenged skin

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