ArticleEMBO molecular medicine2019
Role of bulge epidermal stem cells and TSLP signaling in psoriasis.
Article in EMBO molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Fatty acid-binding protein 5 aggravates psoriasis and psoriasis-like disease through ferroptosis.Cell death and differentiation · 2026Article
- Psoriasis-like disease prevents squamous skin tumor development by neutrophil-driven inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Enhanced Alarmin Secretion Exacerbates Neutrophil Extracellular Trap (NET) Formation in Active Psoriasis: Implication of IL-33 and TSLP in Driving NET Formation, Inflammation and Oxidative Stress in Psoriasis.Antioxidants (Basel, Switzerland) · 2026Article
- Vascular endothelial cells as signaling niches for epithelial stem cells in the skin.Frontiers in cell and developmental biology · 2026Review
- B cell-derived acetylcholine mitigates skin inflammation in mice through α9 nicotinic acetylcholine receptor-mediated signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epidermal stem cells: skin surveillance and clinical perspective.Journal of translational medicine · 2024Review
- The Role of Alarmins in the Pathogenesis of Rheumatoid Arthritis, Osteoarthritis, and Psoriasis.Current issues in molecular biology · 2024Review
- Bombesin receptor-activated protein homolog deficiency altered the pattern of pathological changes of psoriasis - like skin lesion in mice.International journal of medical sciences · 2024Article
- Extracellular serine empowers epidermal proliferation and psoriasis-like symptoms.Science advances · 2022Article
- Targeting the Epithelium-Derived Innate Cytokines: From Bench to Bedside.Immune network · 2022Review
- CB2R Deficiency Exacerbates Imiquimod-Induced Psoriasiform Dermatitis and Itch Through the Neuro-Immune Pathway.Frontiers in pharmacology · 2022Article
- Single-Cell Transcriptomics Uncover Key Regulators of Skin Regeneration in Human Long-Term Mechanical Stretch-Mediated Expansion Therapy.Frontiers in cell and developmental biology · 2022Article
- Role of Epithelium-Derived Cytokines in Atopic Dermatitis and Psoriasis: Evidence and Therapeutic Perspectives.Biomolecules · 2021Review
- Topical application of an amygdalin analogue reduces inflammation and keratinocyte proliferation in a psoriasis mouse model.Experimental dermatology · 2021Article
- The AP-1 transcription factors c-Jun and JunB are essential for CD8α conventional dendritic cell identity.Cell death and differentiation · 2021Article
- Psoriatic skin inflammation is promoted by c-Jun/AP-1-dependent CCL2 and IL-23 expression in dendritic cells.EMBO molecular medicine · 2021Article
- Thymic Stromal Lymphopoietin in Cutaneous Immune-Mediated Diseases.Frontiers in immunology · 2021Review
- Molecular and Cellular Mechanisms of Itch in Psoriasis.International journal of molecular sciences · 2020Review
- Stem Cells as a Target for the Delivery of Active Molecules to Skin by Topical Administration.International journal of molecular sciences · 2020Review
- Role of bulge epidermal stem cells and TSLP signaling in psoriasis.EMBO molecular medicine · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Psoriasis is a common inflammatory skin disease involving a cross-talk between epidermal and immune cells. The role of specific epidermal stem cell populations, including hair follicle stem cells (HF-SCs) in psoriasis is not well defined. Here, we show reduced expression of c-JUN and JUNB in bulge HF-SCs in patients with scalp psoriasis. Using lineage tracing in mouse models of skin inflammation with inducible deletion of c-Jun and JunB, we found that mutant bulge HF-SCs initiate epidermal hyperplasia and skin inflammation. Mechanistically, thymic stromal lymphopoietin (TSLP) was identified in mutant cells as a paracrine factor stimulating proliferation of neighboring non-mutant epidermal cells, while mutant inter-follicular epidermal (IFE) cells are lost over time. Blocking TSLP in psoriasis-like mice reduced skin inflammation and decreased epidermal proliferation, VEGFα expression, and STAT5 activation. These findings unravel distinct roles of HF-SCs and IFE cells in inflammatory skin disease and provide novel mechanistic insights into epidermal cell interactions in inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.