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Do, Yoonkyung
DC-based Immune System & Immunotherapy (DISNI) Lab
Research Interests
  • Study on various subsets of dendritic cells and their immunological functions
  • Vaccine development by targeting pathogenic antigens to distinct DC subsets via anti-DC-subset-specific-receptor monoclonal antibodies
  • Characterization of roles of DCs in tumor microenvironment and tumor metastasis
  • Studies on role of DCs in neuro-related diseases
  • Study DCs in collaboration with Biotechnology or Engineering field

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Targeted deletion of CD44v7 exon leads to decreased endothelial cell injury but not tumor cell killing mediated by interleukin-2-activated cytolytic lymphocytes

DC Field Value Language
dc.contributor.author McKallip, RJ ko
dc.contributor.author Fisher, M ko
dc.contributor.author Do, Yoonkyung ko
dc.contributor.author Szakal, AK ko
dc.contributor.author Gunthert, U ko
dc.contributor.author Nagarkatti, PS ko
dc.contributor.author Nagarkatti, M ko
dc.date.available 2014-10-10T01:58:22Z -
dc.date.created 2014-10-08 ko
dc.date.issued 2003-10 -
dc.identifier.citation JOURNAL OF BIOLOGICAL CHEMISTRY, v.278, no.44, pp.43818 - 43830 ko
dc.identifier.issn 0021-9258 ko
dc.identifier.uri https://scholarworks.unist.ac.kr/handle/201301/7068 -
dc.identifier.uri http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0242384768 ko
dc.description.abstract In the current study, we investigated the nature and role of CD44 variant isoforms involved in endothelial cell (EC) injury and tumor cell cytotoxicity mediated by IL-2-activated killer (LAK) cells. Treatment of CD44 wild-type lymphocytes with IL-2 led to increased gene expression of CD44 v6 and v7 variant isoforms and to significant induction of vascular leak syndrome (VLS). CD44v6-v7 knockout (KO) and CD44v7 KO mice showed markedly reduced levels of IL-2-induced VLS. The decreased VLS in CD44v6-v7 KO and CD44v7 KO mice did not result from differential activation and expansion of CD8(+) T cells, NK, and NK-T cells or from altered degree of perivascular lymphocytic infiltration in the lungs. LAK cells from CD44v7 KO mice showed a significant decrease in their ability to adhere to and mediate lysis of EC but not lysis of P815 tumor cells in vitro. CD44v7-mediated lysis of EC by LAK cells was dependent on the activity of phosphatidylinositol 3-kinase and tyrosine kinases. Interestingly, IL-2-activated LAK cells expressing CD44(hi) but not CD44(lo) were responsible for EC lysis. Furthermore, lysis of EC targets could be blocked by addition of soluble or enzymatic cleavage of CD44v6-v7-binding glycosaminoglycans. Finally, anti-CD44v7 mAbs caused a significant reduction in the adherence to and killing of EC and led to suppression of IL-2-induced VLS. Together, this study suggests that the expression of CD44v7 on LAK cells plays a specific role in EC injury and that it may be possible to reduce EC injury but not tumor cell killing by specifically targeting CD44v7. ko
dc.description.statementofresponsibility close -
dc.language ENG ko
dc.publisher AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC ko
dc.subject DOSE RECOMBINANT INTERLEUKIN-2 ko
dc.subject DELAYED-TYPE HYPERSENSITIVITY ko
dc.subject ADHESION MOLECULES ko
dc.subject T-CELLS ko
dc.subject VARIANT ISOFORMS ko
dc.subject HYALURONIC-ACID ko
dc.subject KILLER-CELLS ko
dc.subject MICE ko
dc.subject INVOLVEMENT ko
dc.subject TOXICITY ko
dc.title Targeted deletion of CD44v7 exon leads to decreased endothelial cell injury but not tumor cell killing mediated by interleukin-2-activated cytolytic lymphocytes ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-0242384768 ko
dc.identifier.wosid 000186157000132 ko
dc.type.rims ART ko
dc.description.wostc 18 *
dc.description.scopustc 19 *
dc.date.tcdate 2015-05-06 *
dc.date.scptcdate 2014-10-08 *
dc.identifier.doi 10.1074/jbc.M304467200 ko
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