CD27 engagement by a soluble CD70 protein enhances non-cytolytic antiviral activity of CD56bright natural killer cells by IFN-γ secretion

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dc.contributor.authorY S Jang-
dc.contributor.authorW Kang-
dc.contributor.authorD Y Chang-
dc.contributor.authorP S Sung-
dc.contributor.authorBum Chan Park-
dc.contributor.authorS H Yoo-
dc.contributor.authorYoung Woo Park-
dc.contributor.authorE C Shin-
dc.date.accessioned2017-04-19T09:48:01Z-
dc.date.available2017-04-19T09:48:01Z-
dc.date.issued2013-
dc.identifier.issn1521-6616-
dc.identifier.uri10.1016/j.clim.2013.09.007ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11727-
dc.description.abstractWe investigated regulation of human NK cell function by CD27 engagement using a recombinant soluble CD70 protein. CD27 was preferentially expressed on CD56bright NK cells, and soluble CD70 protein bound to CD27+CD56bright NK cells. While soluble CD70 protein enhanced IFN-γ secretion by CD56bright NK cells in the presence of IL-12, it augmented neither cytolytic activity nor proliferation of NK cells. Thus, we next asked if soluble CD70 protein could be used to induce non-cytolytic antiviral activity of NK cells using an in vitro hepatitis C virus (HCV) infection system. Soluble CD70 protein stimulated NK cells to suppress HCV replication by enhancing NK cell IFN-γ secretion without killing infected cells. Taken together, we demonstrate that CD27 engagement by a soluble CD70 protein enhances non-cytolytic antiviral activity of CD56bright NK cells by IFN-γ secretion. Thus, this soluble CD70 protein may be useful for the treatment of viral infections such as HCV infection.-
dc.publisherElsevier-
dc.titleCD27 engagement by a soluble CD70 protein enhances non-cytolytic antiviral activity of CD56bright natural killer cells by IFN-γ secretion-
dc.title.alternativeCD27 engagement by a soluble CD70 protein enhances non-cytolytic antiviral activity of CD56bright natural killer cells by IFN-γ secretion-
dc.typeArticle-
dc.citation.titleClinical Immunology-
dc.citation.number3-
dc.citation.endPage387-
dc.citation.startPage379-
dc.citation.volume149-
dc.contributor.affiliatedAuthorBum Chan Park-
dc.contributor.affiliatedAuthorYoung Woo Park-
dc.contributor.alternativeName장영순-
dc.contributor.alternativeName강원석-
dc.contributor.alternativeName장동엽-
dc.contributor.alternativeName성필수-
dc.contributor.alternativeName박범찬-
dc.contributor.alternativeName유석호-
dc.contributor.alternativeName박영우-
dc.contributor.alternativeName신의철-
dc.identifier.bibliographicCitationClinical Immunology, vol. 149, no. 3, pp. 379-387-
dc.identifier.doi10.1016/j.clim.2013.09.007-
dc.subject.keywordCD27-
dc.subject.keywordCD70-
dc.subject.keywordHepatitis C virus-
dc.subject.keywordIFN-γ-
dc.subject.keywordNatural killer cells-
dc.subject.localCD27-
dc.subject.localCD70-
dc.subject.localhepatitis C virus-
dc.subject.localHepatitis C virus-
dc.subject.localIFN-γ-
dc.subject.localIfn-γ-
dc.subject.localIFN-gamma-
dc.subject.localNatural killer cell-
dc.subject.localNatural killer cells-
dc.subject.localnatural killer (NK) cells-
dc.subject.localnatural killer cell-
dc.description.journalClassY-
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