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DC Field | Value | Language |
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dc.citation.endPage | 43830 | - |
dc.citation.number | 44 | - |
dc.citation.startPage | 43818 | - |
dc.citation.title | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.citation.volume | 278 | - |
dc.contributor.author | McKallip, RJ | - |
dc.contributor.author | Fisher, M | - |
dc.contributor.author | Do, Yoonkyung | - |
dc.contributor.author | Szakal, AK | - |
dc.contributor.author | Gunthert, U | - |
dc.contributor.author | Nagarkatti, PS | - |
dc.contributor.author | Nagarkatti, M | - |
dc.date.accessioned | 2023-12-22T11:09:07Z | - |
dc.date.available | 2023-12-22T11:09:07Z | - |
dc.date.created | 2014-10-08 | - |
dc.date.issued | 2003-10 | - |
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. | - |
dc.identifier.bibliographicCitation | JOURNAL OF BIOLOGICAL CHEMISTRY, v.278, no.44, pp.43818 - 43830 | - |
dc.identifier.doi | 10.1074/jbc.M304467200 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.scopusid | 2-s2.0-0242384768 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/7068 | - |
dc.identifier.url | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0242384768 | - |
dc.identifier.wosid | 000186157000132 | - |
dc.language | 영어 | - |
dc.publisher | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC | - |
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 | - |
dc.type | Article | - |
dc.description.journalRegisteredClass | scopus | - |
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