Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A transcriptomic atlas of murine and human alopecia areata identifies immune cell profiles predictive of human disease state.

ABSTRACT: Alopecia areata (AA) is one of the most common autoimmune conditions, presenting initially with loss of hair without overt skin changes. The unremarkable appearance of the skin surface contrasts with the complex immune activity occurring at the hair follicle. AA pathogenesis is due to the loss of immune privilege of the hair follicle leading to autoimmune attack. Although the literature has focused on CD8+ T cells, vital roles for CD4+ T cells and antigen-presenting cells have been suggested. Here, we use single-cell sequencing to reveal distinct expression profiles of immune cells in AA. We found clonal expansions of both CD4+ and CD8+ T cells, with shared clonotypes across varied transcriptional states. These data were used to generate highly predictive models of human AA disease. Finally, single-cell sequencing of T cells in human AA recapitulated the clonotypic findings and the gene expression of the predictive models.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE145095 | GEO | 2020/08/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Alopecia areata susceptibility variant in MHC region impacts expressions of genes contributing to hair keratinization and is involved in hair loss

Project description:Background: Alopecia areata (AA) is considered a highly heritable, T-cell-mediated autoimmune disease of the hair follicle. However, no convincing susceptibility gene has yet been pinpointed in the major histocompatibility complex (MHC), a genome region known to be associated with AA as compared to other regions. Methods: We engineered mice carrying AA risk allele identified by haplotype sequencing for the MHC region using allele-specific genome editing with the CRISPR/Cas9 system. Finally, we performed functional evaluations in the mice and AA patients with and without the risk allele. Findings: We identified a variant (rs142986308, p.Arg587Trp) in the coiled-coil alpha-helical rod protein 1 (CCHCR1) gene as the only non-synonymous variant in the AA risk haplotype. Furthermore, mice engineered to carry the risk allele displayed a hair loss phenotype. Transcriptomics further identified CCHCR1 as a novel component interacting with hair cortex keratin in hair shafts. Both, these alopecic mice and AA patients with the risk allele displayed morphologically impaired hair and comparable differential expression of hair-related genes, including hair keratin and keratin-associated proteins (KRTAPs). Interpretation: Our results implicate CCHCR1 with the risk allele in a previously unidentified subtype of AA based on aberrant keratinization in addition to autoimmune events.

2021-12-31 | GSE149653 | GEO

RNAseq of organ-cultured human hair follicles exposed to MEKi (Cobimetinib)

Project description:EGFR/MEK inhibitor therapy induces a distinct inflammatory hair follicle response that includes a collapse of hair follicle immune privilege and differential modulation of IL-33 and IL-37 expression. Our findings suggest that successful future management of EGFRi/MEKi-induced folliculitis requires restoration of hair follicle immune privilege. In this RNAseq organ-cultured human hair follicles were directly exposed to MEKi (Cobimetinib) or the control DMSO (n=5 patients (6-8 hair follicles per patient)).

2024-07-19 | E-MTAB-13454 | biostudies-arrayexpress

Spatial transcriptomics of autoimmune alopecia

Project description:Autoimmune alopecia is a prevalent, highly morbid disease. The inflammatory pathways causing hair loss are not well characterized. We profiled two tissue microarrays comparing healthy skin to scarring alopecia and alopecia areata via spatial transcriptomics to analyze the genes and pathways dysregulated in autoimmune alopecia in direct proximity to the hair follicle.

2023-09-25 | GSE227632 | GEO

RNAseq of scalp biopsies from EGFRi treated patients, who exhibited a folliculitis

Project description:EGFR/MEK inhibitor therapy induces a distinct inflammatory hair follicle response that includes a collapse of hair follicle immune privilege and differential modulation of IL-33 and IL-37 expression. Our findings suggest that successful future management of EGFRi/MEKi-induced folliculitis requires restoration of hair follicle immune privilege. In this RNAseq parietal scalp (rather than truncal skin) biopsies were taken from long-term (3-9 months) EGFRi-treated patients exhibiting folliculitis (Chronic-EGFRi) or from patients prior to commencing and after two weeks of EGFRi therapy (Acute-EGFRi), compared to normal scalp skin.

2024-07-19 | E-MTAB-13455 | biostudies-arrayexpress

Less invasive diagnostics for cancer using hair follicle

Project description:Primary outcome(s): Comparison of the gene expression profile in hair follicle between cancer patients and healthy volunteer

| 2628246 | ecrin-mdr-crc

JAK-STAT1 as therapeutic target for EGFR deficiency-associated inflammation and scarring alopecia (RNA-seq of HFSC)

Project description:The hair follicle stem cell niche is an immune-privileged microenvironment, characterized by reduced antigen presentation, thus shielding against permanent immune-mediated tissue damage. In this study, we demonstrated the protective role of hair follicle-specific epidermal growth factor receptor (EGFR) against scarring hair follicle destruction. Mechanistically, disruption of EGFR signalling generated a cell-intrinsic hypersensitivity within the JAK-STAT1 pathway, which, synergistically with interferon gamma expressing CD8 T-cell and NK-cell-mediated inflammation, compromised the stem cell niche. Hair follicle-specific genetic depletion of either JAK1/2 or STAT1 or therapeutic inhibition of JAK1/2 ameliorated the inflammation, restored skin barrier function and activated the residual stem cells to resume hair growth in mouse models of epidermal and hair follicle-specific EGFR deletion. Skin biopsies from EGFR inhibitor-treated and cicatricial alopecia patients indicated active STAT1 signalling and interferon target expression. Notably, a case study of folliculitis decalvans, characterized by progressive hair loss, scaling and perifollicular erythema, demonstrated successful treatment with JAK1/2 inhibition. Our findings offer molecular insights and present a mechanism-based therapeutic strategy for addressing chronic folliculitis associated with EGFR-inhibitor anti-cancer therapy and cicatricial alopecia.

2024-07-31 | GSE273571 | GEO

JAK-STAT1 as therapeutic target for EGFR deficiency-associated inflammation and scarring alopecia (scRNA-seq)

2024-07-31 | GSE273572 | GEO

Hair follicle stem cells sense niche integrity and recruit immune cells to contain barrier breaches

Project description:We demonstrated that hair follicle stem cells (HFSCs) are able to sense the integrity of their epithelial niche. By ablating a core cell junction component E-cadherin (encoded by Cdh1), the epithelial niche no longer maintains proper barrier function, leading to microbial infiltration through the hair follicle. The surrounding HFSCs respond by increasing its expression of immune associated genes and recruiting immune cells to their niche so as to cope with compromised tissue function.

2018-12-28 | GSE106767 | GEO

mice，skin, iTRAQ

Project description:Wound Induced Hair Follicle neogenesis (WIHN) is a hair neogenesis phenomenon which occurred in the center of scar. Neonatal hair follicle are separated from the preexisting follicles by a hairless circular. We analysed the differentially expressed proteins between inner and outer area of scar at post-wound day 15 by iTRAQ technology.

2021-09-08 | PXD012868 | Pride

Calcineurin/Nfatc1 links skin stem cell quiescence to the endocrine hormone prolactin

Project description:Cyclosporine A (CSA) leads to the precocious onset of hair follicle growth, which is driven by premature activation and proliferation of hair follicle stem cells. Here, we identify gene expression changes associated with CSA treatment in hair follicle stem cells prior to the onset of proliferation as a readout for the early events in stem cell actvation. Hair follicle bulge stem cells were FACS-isolated from mouse skin during the 2nd telogen. Two biological replicated were performed.

2013-09-27 | E-GEOD-51194 | biostudies-arrayexpress

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