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    <IdentifierUrn>urn:nbn:de:0183-25rhk1277</IdentifierUrn>
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      <Title language="en">Identification of a cytotoxic CD4&#43; T Cell population in juvenile idiopathic arthritis</Title>
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          <Lastname>M&#252;ller</Lastname>
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          <Affiliation>Klinik und Poliklinik f&#252;r Kinder- und Jugendmedizin, p&#228;diatrische Immunologie, Kinderrheumatologie und -infektiologie, Leipzig</Affiliation>
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          <Affiliation>Klinik und Poliklinik f&#252;r Kinder- und Jugendmedizin, p&#228;diatrische Immunologie, Kinderrheumatologie und -infektiologie, Leipzig</Affiliation>
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          <Affiliation>Klinik und Poliklinik f&#252;r Endokrinologie, Nephrologie und Rheumatologie, Rheumatologie, Leipzig</Affiliation>
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          <Affiliation>Klinik und Poliklinik f&#252;r Endokrinologie, Nephrologie und Rheumatologie, Rheumatologie, Leipzig</Affiliation>
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          <Corporatename>German Medical Science GMS Publishing House</Corporatename>
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        <Address>D&#252;sseldorf</Address>
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      <SubjectheadingDDB>610</SubjectheadingDDB>
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    <DatePublishedList>
      <DatePublished>20250917</DatePublished>
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    <Language>engl</Language>
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      <AltText language="en">This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License.</AltText>
      <AltText language="de">Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung).</AltText>
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      <Meeting>
        <MeetingId>M0627</MeetingId>
        <MeetingSequence>127</MeetingSequence>
        <MeetingCorporation>Deutsche Gesellschaft f&#252;r Rheumatologie</MeetingCorporation>
        <MeetingCorporation>Deutsche Gesellschaft f&#252;r Orthop&#228;dische Rheumatologie</MeetingCorporation>
        <MeetingName>53. Kongress der Deutschen Gesellschaft f&#252;r Rheumatologie (DGRh), 39. Jahrestagung der Deutschen Gesellschaft f&#252;r Orthop&#228;dische Rheumatologie (DGORh)</MeetingName>
        <MeetingTitle>Deutscher Rheumatologiekongress 2025</MeetingTitle>
        <MeetingSession>Kinderrheumatologie</MeetingSession>
        <MeetingCity>Wiesbaden</MeetingCity>
        <MeetingDate>
          <DateFrom>20250917</DateFrom>
          <DateTo>20250920</DateTo>
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    <ArticleNo>KI.04</ArticleNo>
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      <MainHeadline>Text</MainHeadline><Pgraph><Mark1>Introduction: </Mark1>Juvenile idiopathic arthritis (JIA) describes a heterogeneous group of several subtypes of chronic, autoimmune diseases characterized by an ongoing inflammation of the joints under the age of 16 <TextLink reference="1"></TextLink>. While the subtypes differ in symptoms, therapy and pathogenesis, research has established a crucial role of CD4&#43; T cells in the pathogenesis of multiple subtypes <TextLink reference="2"></TextLink>. SLAMF7 is a marker found on immune cells like NK cells and CD8&#43; T cells and is associated with cytotoxicity <TextLink reference="3"></TextLink>, <TextLink reference="4"></TextLink>. Since cytotoxic CD4&#43; T cell populations (CD4 CTL) play an increasing role in inflammatory diseases, we were interested if CD4 CTLs are already detectable in JIA.</Pgraph><Pgraph><Mark1>Methods: </Mark1>We isolated peripheral blood mononuclear cells (PBMCs) of children with JIA and a healthy age matched control group (HC) by using Ficoll density gradient. The PBMCs were stained for expression of surface markers (CD3, CD8, CD4, SLAMF7, CCR7, CD27, HLA-DR) and the intracellular marker Granzyme A. Cells were acquired on FACS LSR Fortessa (BD Biosciences) and analyzed using FlowJo V10 software.</Pgraph><Pgraph><Mark1>Results: </Mark1>CD4&#43; T cells of children with JIA (n&#61;27, p&#61; 0.0202) showed a significantly higher expression of SLAMF7 on the surface compared to HC (n&#61;3). Next, we analyzed SLAMF7&#43; on na&#239;ve, central memory and effector-memory CD4&#43; T cells, based on the expression of CCR7 and CD27. Especially na&#239;ve CD4&#43; T cells (CCR7&#43;CD27&#43;), showed a significantly higher expression of SLAMF7 in contrast to na&#239;ve CD4&#43; T cells of HC. Furthermore, SLAMF7&#43;CD4&#43; T cells revealed a higher expression of Granzyme A and activation marker HLA-DR than their SLAMF7-CD4&#43; T cell counterparts and CD4&#43; T cells of HC.</Pgraph><Pgraph><Mark1>Conclusion: </Mark1>In summary, we found an increased SLAMF7&#43;CD4&#43; T cell population with potentially cytotoxic features. Since, SLAMF7 can act as an inhibitor or activator for immune cells, further investigations are necessary to examine the role of SLAMF7&#43;CD4&#43; T cells in the pathogenesis of JIA. </Pgraph><Pgraph>The association between SLAMF7 expression and increased Granzyme A and HLA-DR levels implies that SLAMF7 may play a role in regulating T cell activation and effector functions in both health and disease states. To enhance our comprehension of this mechanism, an analysis of synovial fluid would be beneficial.</Pgraph><Pgraph><Mark1>Disclosures: </Mark1>The authors and I declare that the research was conducted in the absence of financial or commercial relationships that could be construed as a potential conflict of interest.</Pgraph></TextBlock>
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