Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7217070.fastq.gz | Fastqsanger.gz | |||
| SRR7217080.fastq.gz | Fastqsanger.gz | |||
| SRR7217090.fastq.gz | Fastqsanger.gz | |||
| SRR7217100.fastq.gz | Fastqsanger.gz | |||
| SRR7217110.fastq.gz | Fastqsanger.gz |
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Project description:Scalp psoriasis shows a variable clinical spectrum and in many cases poses a great therapeutic challenge. However, it remains unknown whether the immune response of scalp psoriasis differs from understood pathomechanisms of psoriasis on other skin areas. We sought to determine the cellular and mollecular phenotype of scalp psoriasis by performing a comparative analysis of scalp vs skin using lesional and nonlesional samples from 20 Caucasian subjects with untreated moderate to severe psoriasis and significant scalp involvement, and 10 control subjects without psoriasis. Our results suggest that even in the scalp psoriasis is a disease of the inter-follicular skin. The immune mechanisms that mediate scalp psoriasis were found to be similar to those involved in skin psoriasis. However, the magnitude of dysregulation, number of differentially expressed genes, and enrichment of the psoriatic genomic fingerprinting were more prominent in skin lesions. Furthermore, the scalp transcriptome showed increased modulation of several gene-sets, particularly those induced by interferon-gamma, compared with skin psoriasis which was mainly associated with activation of TNFâµ/L-17/IL-22-induced keratinocyte response genes. We also detected differences in expression of gene-sets involving negative regulation, epigenetic regulation, epidermal differentiation, and dendritic cell or Th1/Th17/Th22-related T-cell processes. To define the transcriptomic profile of scalp skin, punch biopsies (6 mm diameter) were obtained from 20 Caucasian patients with untreated moderate to severe psoriasis with significative scalp involvement and 10 control subjects without psoriasis (N). Lesional (LS) samples were isolated from the infiltrated border of a plaque of psoriasis. Non lesional (NL) samples were taken from scalp areas with no visible psoriasis between the infiltrated plaques.
2015-11-25 | E-GEOD-75343 | biostudies-arrayexpress
Project description:Three individual patient-originated (Scalp trauma; ages 37, 46 and 57) DPCs were used for the studies. Dermal papilla cells, derived from the frontal scalp of 3 women, were treated with normal medium (Ctrl group) and medium containing 10-7 M corticotropin-releasing hormone (CRH group) for 72 h. Proteins were extracted and digested with trypsin for 4D label-free quantitative proteomics (Shanghai Applied Protein Technology Co., Ltd.).
2025-05-07 | PXD057745 | Pride
Project description:Background: Scalp psoriasis presents distinct clinical features and treatment resistance compared to lesions on other body sites, yet its immune landscape remains poorly characterized. Methods: We performed single-cell RNA sequencing (scRNA-seq) on CD45⁺ immune cells from scalp and body plaque lesions of psoriasis patients and healthy controls. A total of 41,438 immune cells were analyzed. Downstream analyses included clustering, gene set enrichment, pseudotime trajectory inference, and cell–cell interaction modeling. Multiplex immunofluorescence was used to validate spatial co-localization. Results: Scalp psoriasis lesions exhibited a higher abundance of IL17⁺ CD8⁺ tissue-resident memory T (Tc17) cells, which co-expressed IFNG and lipid transporter FATP2 (SLC27A2). Pseudotime analysis revealed a trajectory from IL7R⁺ Trm cells toward Tc17 cells, especially enriched in the scalp. Trem2⁺ macrophages in scalp lesions showed increased expression of inflammatory mediators and MHC-I molecules. CellChat revealed enhanced MHC-I–mediated interactions between Trem2⁺ macrophages and Tc17 cells in the scalp. These interactions were confirmed by immunofluorescence, demonstrating co-localization of FATP2⁺ Tc17 and Trem2⁺ macrophages around sebaceous units. Conclusions: This study defines a scalp-specific pathogenic axis involving Trem2⁺ macrophages and FATP2⁺ Tc17 cells, potentially explaining the localization and persistence of inflammation in scalp psoriasis. Targeting lipid metabolism or specific cell–cell interactions may provide new therapeutic avenues for treatment-resistant scalp psoriasis.
2025-07-17 | GSE302456 | GEO
Project description:Scalp Microbiome in Psoriasis Capitis and Healthy Individuals
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Project description:Scalp psoriasis shows a variable clinical spectrum and in many cases poses a great therapeutic challenge. However, it remains unknown whether the immune response of scalp psoriasis differs from understood pathomechanisms of psoriasis on other skin areas. We sought to determine the cellular and mollecular phenotype of scalp psoriasis by performing a comparative analysis of scalp vs skin using lesional and nonlesional samples from 20 Caucasian subjects with untreated moderate to severe psoriasis and significant scalp involvement, and 10 control subjects without psoriasis. Our results suggest that even in the scalp psoriasis is a disease of the inter-follicular skin. The immune mechanisms that mediate scalp psoriasis were found to be similar to those involved in skin psoriasis. However, the magnitude of dysregulation, number of differentially expressed genes, and enrichment of the psoriatic genomic fingerprinting were more prominent in skin lesions. Furthermore, the scalp transcriptome showed increased modulation of several gene-sets, particularly those induced by interferon-gamma, compared with skin psoriasis which was mainly associated with activation of TNF↵/L-17/IL-22-induced keratinocyte response genes. We also detected differences in expression of gene-sets involving negative regulation, epigenetic regulation, epidermal differentiation, and dendritic cell or Th1/Th17/Th22-related T-cell processes.
2015-11-25 | GSE75343 | GEO
Project description:We explore whether a low-energy diet intervention for Metabolic dysfunction-associated steatohepatitis (MASH) improves liver disease by means of modulating the gut microbiome. 16 individuals were given a low-energy diet (880 kcal, consisting of bars, soups, and shakes) for 12 weeks, followed by a stepped re-introduction to whole for an additional 12 weeks. Stool samples were obtained at 0, 12, and 24 weeks for microbiome analysis. Fecal microbiome were measured using 16S rRNA gene sequencing. Positive control (Zymo DNA standard D6305) and negative control (PBS extraction) were included in the sequencing. We found that low-energy diet improved MASH disease without lasting alterations to the gut microbiome.
2024-12-31 | E-MTAB-14061 | biostudies-arrayexpress