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EMBO Mol Med. 2019 Nov 7;11(11):e10697. doi: 10.15252/emmm.201910697. Epub 2019 Sep 26.

Role of bulge epidermal stem cells and TSLP signaling in psoriasis.

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Genes, Development and Disease Group, Cancer Cell Biology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Confocal Unit at Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Bioinformatics Unit at Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Tissue Engineering Group, Biodonostia Health Research Institute, San Sebastian, Spain.
Grupo de Patología Médica, Mediteknia Dermatologic Clinic, Universidad Fernando Pessoa Canarias, Universidad Las Palmas Gran Canaria, Las Palmas de Gran Canaria, Spain.
Department of Dermatology and Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.


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.


epidermal hyper-proliferation; hair follicle stem cells; lineage tracing; psoriasis; thymic stromal lymphopoietin

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