<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-14T03:52:38Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/9320" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/9320</identifier><datestamp>2024-11-29T23:04:35Z</datestamp><setSpec>com_20.500.12105_2173</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19597</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Gago-Lopez, Nuria</subfield>
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      <subfield code="a">Mellor Liliana, Mellor Liliana F</subfield>
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      <subfield code="a">Megias Vazquez, Diego</subfield>
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      <subfield code="a">Martín-Serrano, Guillermo</subfield>
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      <subfield code="a">Izeta, Ander</subfield>
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      <subfield code="a">Jimenez, Francisco</subfield>
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      <subfield code="a">Wagner, Erwin Friedrich</subfield>
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      <subfield code="c">2019-11-07</subfield>
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      <subfield code="a">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.</subfield>
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      <subfield code="a">EMBO Mol Med. 2019;11(11):e10697.</subfield>
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      <subfield code="a">10.15252/emmm.201910697</subfield>
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      <subfield code="a">EMBO molecular medicine</subfield>
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      <subfield code="a">31556482</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/9320</subfield>
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   <datafield tag="653" ind2=" " ind1=" ">
      <subfield code="a">Epidermal hyper-proliferation</subfield>
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      <subfield code="a">Hair follicle stem cells</subfield>
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      <subfield code="a">Psoriasis</subfield>
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      <subfield code="a">Thymic stromal lymphopoietin</subfield>
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      <subfield code="a">Role of bulge epidermal stem cells and TSLP signaling in psoriasis</subfield>
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