ArticleCell & bioscience2025
Single-cell sequencing combined with spatial transcriptomics reveals the characteristics of follicle-targeted inflammation patterns in primary cicatricial alopecia.
Article in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Single-cell transcriptomics reveals epithelial-stromal crosstalk underlying fibrotic remodeling in frontal fibrosing alopecia.iScience · 2026Article
- The niche-centric view: Redefining inflammatory disease beyond molecular signatures.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026Article
- Hair follicle immune privilege in autoimmune and immune-mediated alopecias: paths toward reestablishing immune tolerance.Frontiers in medicine · 2026Review
- Dendrobium officinale polysaccharide improves hair regrowth in androgenetic alopecia mice and is associated with coordinated changes in local steroid metabolism, ESR1 activation, and keratin-related follicular responses.Frontiers in pharmacology · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundPrimary cicatricial alopecia (PCA) causes irreversible hair loss due to immune-mediated hair follicle destruction. This study investigates follicle-targeted inflammation in lichen planopilaris (LPP), a major PCA subtype, to identify therapeutic targets.
methodsScalp samples from LPP, localized scleroderma (LS), and controls were analyzed using single-cell RNA sequencing and spatial transcriptomics. Cellular composition, spatial localization, and intercellular interactions were examined using differential gene expression and ligand-receptor analyses.
resultsCD8⁺ effector memory T cells (Tem) and macrophages infiltrated hair follicles in LPP, disrupting immune privilege and promoting scarring. Heightened interferon-γ (IFN-γ) signaling and STAT1 activation in Tem cells caused epithelial-mesenchymal transition (EMT) in hair follicle stem cells (HFSCs). Additionally, macrophage-secreted oncostatin M (OSM) impaired HFSC integrity. These mechanisms drive LPP's inflammation and fibrosis.
conclusionsOur findings identify interferon-γ and oncostatin M as key drivers of LPP pathogenesis, offering targets to reduce follicular scarring and preserve hair growth.
trial registrationNot applicable.
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