@article{DelRioOliva2022-12-14Immun-59567,
  year={2022},
  doi={10.3389/fimmu.2022.1075615},
  title={Immunoproteasome inhibition attenuates experimental psoriasis},
  volume={13},
  journal={Frontiers in Immunology},
  author={Del Rio Oliva, Marta and Mellett, Mark and Basler, Michael},
  note={Article Number: 1075615}
}

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    <dcterms:abstract xml:lang="eng">Introduction: Psoriasis is an autoimmune skin disease associated with multiple comorbidities. The immunoproteasome is a special form of the proteasome expressed in cells of hematopoietic origin.&lt;br /&gt;&lt;br /&gt;Methods: The therapeutic use of ONX 0914, a selective inhibitor of the immunoproteasome, was investigated in Card14ΔE138&lt;sup&gt;+/-&lt;/sup&gt; mice, which spontaneously develop psoriasis-like symptoms, and in the imiquimod murine model.&lt;br /&gt;&lt;br /&gt;Results: In both models, treatment with ONX 0914 significantly reduced skin thickness, inflammation scores, and pathological lesions in the analyzed skin tissue. Furthermore, immunoproteasome inhibition normalized the expression of several pro-inflammatory genes in the ear and significantly reduced the inflammatory infiltrate, accompanied by a significant alteration in the αβ&lt;sup&gt;+&lt;/sup&gt; and γδ&lt;sup&gt;+&lt;/sup&gt; T cell subsets.&lt;br /&gt;&lt;br /&gt;Discussion: ONX 0914 ameliorated psoriasis-like symptoms in two different murine psoriasis models, which supports the use of immunoproteasome inhibitors as a therapeutic treatment in psoriasis.</dcterms:abstract>
    <dc:creator>Del Rio Oliva, Marta</dc:creator>
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    <dc:rights>Attribution 4.0 International</dc:rights>
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    <dcterms:title>Immunoproteasome inhibition attenuates experimental psoriasis</dcterms:title>
    <dc:language>eng</dc:language>
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    <dc:contributor>Del Rio Oliva, Marta</dc:contributor>
    <dcterms:issued>2022-12-14</dcterms:issued>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2022-12-20T10:11:38Z</dc:date>
    <dc:contributor>Mellett, Mark</dc:contributor>
    <dc:creator>Basler, Michael</dc:creator>
    <dc:creator>Mellett, Mark</dc:creator>
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    <dc:contributor>Basler, Michael</dc:contributor>
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