1 Ocak 2019 Dergi makalesi Açık Erişim

Oran, D. C.; Lokumcu, T.; Inceoglu, Y.; Akolpoglu, M. B.; Albayrak, O.; Bal, T.; Kurtoglu, M.; Erkan, M.; Can, F.; Bagci-Onder, T.; Kizilel, S.

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/71561</identifier>
  <creators>
    <creator>
      <creatorName>Oran, D. C.</creatorName>
      <givenName>D. C.</givenName>
      <familyName>Oran</familyName>
      <affiliation>Koc Univ, Biomed Sci &amp; Engn, TR-34450 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Lokumcu, T.</creatorName>
      <givenName>T.</givenName>
      <familyName>Lokumcu</familyName>
      <affiliation>Koc Univ, Biomed Sci &amp; Engn, TR-34450 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Inceoglu, Y.</creatorName>
      <givenName>Y.</givenName>
      <familyName>Inceoglu</familyName>
      <affiliation>Koc Univ, Chem &amp; Biol Engn, TR-34450 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Akolpoglu, M. B.</creatorName>
      <givenName>M. B.</givenName>
      <familyName>Akolpoglu</familyName>
      <affiliation>Koc Univ, Chem &amp; Biol Engn, TR-34450 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Albayrak, O.</creatorName>
      <givenName>O.</givenName>
      <familyName>Albayrak</familyName>
      <affiliation>Koc Univ, Sch Med, Med Microbiol, TR-34450 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Bal, T.</creatorName>
      <givenName>T.</givenName>
      <familyName>Bal</familyName>
      <affiliation>Koc Univ, Biomed Sci &amp; Engn, TR-34450 Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Kurtoglu, M.</creatorName>
      <givenName>M.</givenName>
      <familyName>Kurtoglu</familyName>
    </creator>
    <creator>
      <creatorName>Erkan, M.</creatorName>
      <givenName>M.</givenName>
      <familyName>Erkan</familyName>
    </creator>
    <creator>
      <creatorName>Can, F.</creatorName>
      <givenName>F.</givenName>
      <familyName>Can</familyName>
    </creator>
    <creator>
      <creatorName>Bagci-Onder, T.</creatorName>
      <givenName>T.</givenName>
      <familyName>Bagci-Onder</familyName>
    </creator>
    <creator>
      <creatorName>Kizilel, S.</creatorName>
      <givenName>S.</givenName>
      <familyName>Kizilel</familyName>
    </creator>
  </creators>
  <titles>
    <title>Engineering Human Stellate Cells For Beta Cell Replacement Therapy Promotes In Vivo Recruitment Of Regulatory T Cells</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2019</publicationYear>
  <dates>
    <date dateType="Issued">2019-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/71561</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1016/j.mtbio.2019.100006</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">Type 1 diabetes (T1D) is an autoimmune disease characterized by destruction of pancreatic beta cells. One of the promising therapeutic approaches in T1D is the transplantation of islets; however, it has serious limitations. To address these limitations, immunotherapeutic strategies have focused on restoring immunologic tolerance, preventing transplanted cell destruction by patients' own immune system. Macrophage-derived chemokines such as chemokine-ligand-22 (CCL22) can be utilized for regulatory T cell (Treg) recruitment and graft tolerance. Stellate cells (SCs) have various immunomodulatory functions: recruitment of Tregs and induction of T-cell apoptosis. Here, we designed a unique immune-privileged microenvironment around implantable islets through overexpression of CCL22 proteins by SCs. We prepared pseudoislets with insulin-secreting mouse insulinoma-6 (MIN6) cells and human SCs as a model to mimic naive islet morphology. Our results demonstrated that transduced SCs can secrete CCL22 and recruit Tregs toward the implantation site in vivo. This study is promising to provide a fundamental understanding of SC-islet interaction and ligand synthesis and transport from SCs at the graft site for ensuring local immune tolerance. Our results also establish a new paradigm for creating tolerable grafts for other chronic diseases such as diabetes, anemia, and central nervous system (CNS) diseases, and advance the science of graft tolerance.</description>
  </descriptions>
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