<?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>2026-04-14T05:09:21Z</responseDate><request verb="GetRecord" identifier="oai:www.recercat.cat:2445/171181" metadataPrefix="marc">https://recercat.cat/oai/request</request><GetRecord><record><header><identifier>oai:recercat.cat:2445/171181</identifier><datestamp>2025-12-04T19:02:32Z</datestamp><setSpec>com_2072_1057</setSpec><setSpec>col_2072_478777</setSpec><setSpec>col_2072_478917</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Tiirikainen, Minna Lund</subfield>
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      <subfield code="a">Woetmann, Anders</subfield>
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      <subfield code="a">Norsgaard, Hanne</subfield>
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      <subfield code="a">Santamaria Babí, Luis F.</subfield>
      <subfield code="e">author</subfield>
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      <subfield code="a">Lovato, Paola</subfield>
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   <datafield ind2=" " ind1=" " tag="260">
      <subfield code="c">2020-10-13T14:23:03Z</subfield>
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   <datafield ind2=" " ind1=" " tag="260">
      <subfield code="c">2020-10-13T14:23:03Z</subfield>
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      <subfield code="c">2019-12-27</subfield>
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      <subfield code="c">2020-10-13T14:23:03Z</subfield>
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      <subfield code="a">Background: Psoriasis is a chronic, inflammatory skin disorder resulting from a complex interplay between immune and skin cells via release of soluble mediators. While a lot is known about the molecular mechanisms behind psoriasis pathogenesis, there is still a need for preclinical research models that accuratelyreplicate the disease. Objective: This study aimed to develop and characterize ex vivo culture of psoriasis skin as a model for pharmacological testing, where the immunological events of psoriasis can be followed. Methods: Full thickness punch biopsies of lesional psoriasis skin were cultured in submerged conditions up to 144 h followingin situ T cell stimulation with rhIL-23 and anti-CD3 and anti-CD28 antibodies. The Tcell mediated skin inflammation was assessed by gene and protein l analysis for a panel of inflammatory mediators. Tissue integrity and morphology were evaluated by histological analysis. Results: T cell stimulation resulted in functional and psoriasis specificin situ activation of T cells. The expression levels of most of the proinflammatory mediators related to both immune and skin cells were comparable to these in freshly isolated tissue at 48 and 96 h of culture. Tissue integrity and morphology were sustained up to 96 h. Treatment with a corticosteroid reduced the expression of several proinflammatory cytokines and chemokines, whereas anti-IL-17A antibody treatment reduced the expression of the IL-17A downstream markers IL-8 and DEFB4. Conclusion: By preserving keyimmunopathological mechanisms of psoriasis, ex vivo culture of psoriasis skin can be used for the investigation of inflammatory processes of psoriasis and for preclinical drug discovery research.</subfield>
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      <subfield code="a">Psoriasi</subfield>
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      <subfield code="a">Immunoregulació</subfield>
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      <subfield code="a">Psoriasis</subfield>
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      <subfield code="a">Immunoregulation</subfield>
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      <subfield code="a">Ex vivo culture of lesional psoriasis skin for pharmacological testing</subfield>
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