1 Ocak 2018 Dergi makalesi Açık Erişim

Tahrali, Ilhan; Kucuksezer, Umut Can; Altintas, Ayse; Uygunoglu, Ugur; Akdeniz, Nilgun; Aktas-Cetin, Esin; Deniz, Gunnur

DataCite XML

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/34205</identifier>
  <creators>
    <creator>
      <creatorName>Tahrali, Ilhan</creatorName>
      <givenName>Ilhan</givenName>
      <familyName>Tahrali</familyName>
      <affiliation>Istanbul Univ, Aziz Sancar Inst Expt Med, Dept Immunol, Vakif Gureba St, TR-34093 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Kucuksezer, Umut Can</creatorName>
      <givenName>Umut Can</givenName>
      <familyName>Kucuksezer</familyName>
      <affiliation>Istanbul Univ, Aziz Sancar Inst Expt Med, Dept Immunol, Vakif Gureba St, TR-34093 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Altintas, Ayse</creatorName>
      <givenName>Ayse</givenName>
      <familyName>Altintas</familyName>
      <affiliation>Istanbul Univ, Cerrahpasa Fac Med, Dept Neurol, Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Uygunoglu, Ugur</creatorName>
      <givenName>Ugur</givenName>
      <familyName>Uygunoglu</familyName>
      <affiliation>Istanbul Univ, Cerrahpasa Fac Med, Dept Neurol, Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Akdeniz, Nilgun</creatorName>
      <givenName>Nilgun</givenName>
      <familyName>Akdeniz</familyName>
      <affiliation>Istanbul Univ, Aziz Sancar Inst Expt Med, Dept Immunol, Vakif Gureba St, TR-34093 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Aktas-Cetin, Esin</creatorName>
      <givenName>Esin</givenName>
      <familyName>Aktas-Cetin</familyName>
      <affiliation>Istanbul Univ, Aziz Sancar Inst Expt Med, Dept Immunol, Vakif Gureba St, TR-34093 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Deniz, Gunnur</creatorName>
      <givenName>Gunnur</givenName>
      <familyName>Deniz</familyName>
      <affiliation>Istanbul Univ, Aziz Sancar Inst Expt Med, Dept Immunol, Vakif Gureba St, TR-34093 Istanbul, Turkey</affiliation>
    </creator>
  </creators>
  <titles>
    <title>Dysfunction Of Cd3(-)Cd16(+)Cd56(Dim) And Cd3(-)Cd16(-)Cd56(Bright) Nk Cell Subsets In Rr-Ms Patients</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2018</publicationYear>
  <dates>
    <date dateType="Issued">2018-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/34205</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1016/j.clim.2018.02.005</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">Multiple sclerosis (MS), is a chronic inflammatory disease of central nervous system with unclear etiology. Relapsing-remitting (RR)-MS is the most frequent subtype of disease. Natural Killer (NK) cells have roles in cytotoxicity and immune regulation by cytokine secretions, with uncertain contribution to MS pathogenesis. This study aimed to explore contribution of NK cells to MS pathogenesis. Percentages of CD3(-)CD16(+)CD56(+) total NK cells, CD3(-)CD16(+)CD56(dim) and CD3(-)CD16(-)CD56(bright) NK cell subsets, NK cytotoxicity and intracellular IFN-gamma, IL-10 and IL-22 levels were investigated in patients with RR-MS and clinically isolated syndrome (CIS) as well as healthy subjects. Decreased IFN-gamma and increased IL-22 production might have detrimental effects on the clinical course of RR-MS. Impaired cytotoxicity is correlated with disease duration in RR-MS. These findings support the possible contribution of NK cells to RR-MS immuno-pathogenesis. (C) 2018 Published by Elsevier Inc.</description>
  </descriptions>
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