
<resource xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:datacite="http://datacite.org/schema/kernel-4" xmlns="http://namespace.openaire.eu/schema/oaire/" xsi:schemaLocation="http://namespace.openaire.eu/schema/oaire/ https://www.openaire.eu/schema/repo-lit/4.0/openaire.xsd">
  
<datacite:identifier identifierType="URL">https://phaidra.vetmeduni.ac.at/o:3831</datacite:identifier>

  
<datacite:titles>
  
<datacite:title xml:lang="en">Lack of TYK2 signaling enhances host resistance to Candida albicans skin infection</datacite:title>

  
</datacite:titles>

  
<datacite:creators>
  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Miranda, Sara</datacite:creatorName>

  
<datacite:givenName>Sara</datacite:givenName>

  
<datacite:familyName>Miranda</datacite:familyName>

  
<datacite:affiliation>University of Veterinary Medicine Vienna</datacite:affiliation>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Lassnig, Caroline</datacite:creatorName>

  
<datacite:givenName>Caroline</datacite:givenName>

  
<datacite:familyName>Lassnig</datacite:familyName>

  
<datacite:nameIdentifier nameIdentifierScheme="ORCID" schemeURI="https://orcid.org/">0000-0001-7905-3620</datacite:nameIdentifier>

  
<datacite:affiliation>University of Veterinary Medicine Vienna</datacite:affiliation>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Schmidhofer, Kristina</datacite:creatorName>

  
<datacite:givenName>Kristina</datacite:givenName>

  
<datacite:familyName>Schmidhofer</datacite:familyName>

  
<datacite:affiliation>University of Veterinary Medicine Vienna</datacite:affiliation>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Kjartansdottir, Hrönn</datacite:creatorName>

  
<datacite:givenName>Hrönn</datacite:givenName>

  
<datacite:familyName>Kjartansdottir</datacite:familyName>

  
<datacite:nameIdentifier nameIdentifierScheme="ORCID" schemeURI="https://orcid.org/">0000-0002-2322-3050</datacite:nameIdentifier>

  
<datacite:affiliation>University of Veterinary Medicine Vienna</datacite:affiliation>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Vogl, Claus</datacite:creatorName>

  
<datacite:givenName>Claus</datacite:givenName>

  
<datacite:familyName>Vogl</datacite:familyName>

  
<datacite:nameIdentifier nameIdentifierScheme="ORCID" schemeURI="https://orcid.org/">0000-0002-3996-7863</datacite:nameIdentifier>

  
<datacite:affiliation>University of Veterinary Medicine Vienna</datacite:affiliation>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Tangermann, Simone</datacite:creatorName>

  
<datacite:givenName>Simone</datacite:givenName>

  
<datacite:familyName>Tangermann</datacite:familyName>

  
<datacite:affiliation>University of Veterinary Medicine Vienna</datacite:affiliation>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Tsymala, Irina</datacite:creatorName>

  
<datacite:givenName>Irina</datacite:givenName>

  
<datacite:familyName>Tsymala</datacite:familyName>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Babl, Verena</datacite:creatorName>

  
<datacite:givenName>Verena</datacite:givenName>

  
<datacite:familyName>Babl</datacite:familyName>

  
<datacite:affiliation>University of Veterinary Medicine Vienna</datacite:affiliation>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Müller, Mathias</datacite:creatorName>

  
<datacite:givenName>Mathias</datacite:givenName>

  
<datacite:familyName>Müller</datacite:familyName>

  
<datacite:nameIdentifier nameIdentifierScheme="ORCID" schemeURI="https://orcid.org/">0000-0002-7879-3552</datacite:nameIdentifier>

  
<datacite:affiliation>University of Veterinary Medicine Vienna</datacite:affiliation>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Kuchler, Karl</datacite:creatorName>

  
<datacite:givenName>Karl</datacite:givenName>

  
<datacite:familyName>Kuchler</datacite:familyName>

  
<datacite:nameIdentifier nameIdentifierScheme="ORCID" schemeURI="https://orcid.org/">0000-0003-2719-5955</datacite:nameIdentifier>

  
</datacite:creator>

  
<datacite:creator>
  
<datacite:creatorName nameType="Personal">Strobl, Birgit</datacite:creatorName>

  
<datacite:givenName>Birgit</datacite:givenName>

  
<datacite:familyName>Strobl</datacite:familyName>

  
<datacite:nameIdentifier nameIdentifierScheme="ORCID" schemeURI="https://orcid.org/">0000-0001-5716-3212</datacite:nameIdentifier>

  
<datacite:affiliation>University of Veterinary Medicine Vienna</datacite:affiliation>

  
</datacite:creator>

  
</datacite:creators>

  
<dc:publisher>Nature Portfoliuo</dc:publisher>

  
<resourceType resourceTypeGeneral="literature" uri="http://purl.org/coar/resource_type/c_6501">journal article</resourceType>

  
<datacite:rights rightsURI="http://purl.org/coar/access_right/c_abf2">open access</datacite:rights>

  
<dc:language>eng</dc:language>

  
<dc:description xml:lang="en">Abstract: Candida albicans is the most common human fungal pathogen, causing diseases ranging from local to life-threating systemic infections. Tyrosine kinase 2 (TYK2), a crucial mediator in several cytokine signaling pathways, has been associated with protective functions in various microbial infections. However, its specific contribution in the immune response to fungal infections has remained elusive. In this study, we show that mice lacking TYK2 or its enzymatic activity exhibit enhanced resistance to C. albicans skin infections, limiting fungal spread and accelerating wound healing. Impaired TYK2-signaling prompted the formation of a distinctive layer of necrotic neutrophils around the fungal pathogens. Transcriptomic analysis revealed TYK2&#39;s pivotal role in regulating interferon-inducible genes in neutrophils, thereby impacting their antifungal capacity during infection. Furthermore, we show that TYK2-dependent interferon-gamma (IFN?) production contributes to fungal dissemination from the skin to the kidneys. Our study uncovers a hitherto unrecognized detrimental role of TYK2 in cutaneous C. albicans infections.</dc:description>

  
<datacite:subjects>
  
<datacite:subject xml:lang="en">Signal Transduction</datacite:subject>

  
<datacite:subject xml:lang="en">Animals</datacite:subject>

  
<datacite:subject xml:lang="en">Candida Albicans Immunology</datacite:subject>

  
<datacite:subject xml:lang="en">TYK2 Kinase Metabolism</datacite:subject>

  
<datacite:subject xml:lang="en">TYK2 Kinase Genetics</datacite:subject>

  
<datacite:subject xml:lang="en">Mice</datacite:subject>

  
<datacite:subject xml:lang="en">Interferon-gamma Metabolism</datacite:subject>

  
<datacite:subject xml:lang="en">Interferon-gamma Immunology</datacite:subject>

  
<datacite:subject xml:lang="en">Neutrophils Immunology</datacite:subject>

  
<datacite:subject xml:lang="en">Neutrophils Metabolism</datacite:subject>

  
<datacite:subject xml:lang="en">Mice Knockout</datacite:subject>

  
<datacite:subject xml:lang="en">Mice Inbred C57BL</datacite:subject>

  
<datacite:subject xml:lang="en">Skin Microbiology</datacite:subject>

  
<datacite:subject xml:lang="en">Skin Immunology</datacite:subject>

  
<datacite:subject xml:lang="en">Candidiasis Immunology</datacite:subject>

  
<datacite:subject xml:lang="en">Candidiasis Microbiology</datacite:subject>

  
<datacite:subject xml:lang="en">Candidiasis Genetics</datacite:subject>

  
<datacite:subject xml:lang="en">Female</datacite:subject>

  
<datacite:subject xml:lang="en">Wound Healing Immunology</datacite:subject>

  
<datacite:subject xml:lang="en">Wound Healing Genetics</datacite:subject>

  
<datacite:subject xml:lang="en">Candidiasis Cutaneous Immunology</datacite:subject>

  
<datacite:subject xml:lang="en">Candidiasis Cutaneous Genetics</datacite:subject>

  
<datacite:subject xml:lang="en">Candidiasis, Cutaneous Metabolism</datacite:subject>

  
<datacite:subject xml:lang="en">Candidiasis Cutaneous Microbiology</datacite:subject>

  
<datacite:subject xml:lang="en">Male</datacite:subject>

  
</datacite:subjects>

  
<licenseCondition uri="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</licenseCondition>

  
<file accessRightsURI="http://purl.org/coar/access_right/c_abf2" mimeType="application/pdf" objectType="fulltext">https://phaidra.vetmeduni.ac.at/api/object/o:3831/download</file>

  
<datacite:alternateIdentifiers>
  
<datacite:alternateIdentifier alternateIdentifierType="DOI">10.1038/s41467-024-54888-6</datacite:alternateIdentifier>

  
</datacite:alternateIdentifiers>

  
<datacite:relatedIdentifiers>
  
<datacite:relatedIdentifier relatedIdentifierType="URL" relationType="IsPartOf">https://phaidra.vetmeduni.ac.at/o:605</datacite:relatedIdentifier>

  
</datacite:relatedIdentifiers>

  
<dc:format>application/pdf</dc:format>

  
<dc:source xml:lang="en">Nature Communications</dc:source>

  
<dc:source>issn:2041-1723</dc:source>

  
<version uri="http://purl.org/coar/version/c_970fb48d4fbd8a85">VoR</version>

  
<citationTitle>Nature Communications</citationTitle>

  
<citationVolume>15</citationVolume>

  
<citationIssue>1</citationIssue>

  
<datacite:sizes>
  
<datacite:size>8.63 MB</datacite:size>

  
</datacite:sizes>

  
<datacite:dates>
  
<datacite:date dateType="Issued">2024</datacite:date>

  
</datacite:dates>

  
</resource>