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http://hdl.handle.net/2445/138857
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DC Field | Value | Language |
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dc.contributor.author | Pupuleku, Aldi | - |
dc.contributor.author | Costa García, Marcel | - |
dc.contributor.author | Farré Marimon, Domènec | - |
dc.contributor.author | Hengel, Hartmut | - |
dc.contributor.author | Angulo Aguado, Ana | - |
dc.contributor.author | Muntasell, Aura | - |
dc.contributor.author | López Botet, Miguel | - |
dc.date.accessioned | 2019-08-30T08:09:42Z | - |
dc.date.available | 2019-08-30T08:09:42Z | - |
dc.date.issued | 2017-10-24 | - |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.uri | http://hdl.handle.net/2445/138857 | - |
dc.description.abstract | Human cytomegalovirus (HCMV) infection promotes the differentiation and persistent expansion of a mature NK cell subset, which displays high surface levels of the activating CD94/NKG2C NK cell receptor, together with additional distinctive phenotypic and functional features. The mechanisms underlying the development of adaptive NK cells remain uncertain but some observations support the involvement of a cognate interaction of CD94/NKG2C with ligand(s) displayed by HCMV-infected cells. To approach this issue, the heterodimer and its adaptor (DAP12) were expressed in the human Jurkat leukemia T cell line; signaling was detected by transfection of a reporter plasmid encoding for Luciferase (Luc) under NFAT/AP1-dependent control. Engagement of the receptor by solid-phase bound CD94- or NKG2C-specific monoclonal antibodies (mAbs) triggered Luc expression. Moreover, reporter activation was detectable upon interaction with HLA-E+ 721.221 (.221-AEH) cells, as well as with 721.221 cells incubated with synthetic peptides, which stabilized surface expression of endogenous HLA-E; the response was specifically antagonized by soluble NKG2C- and HLA-E-specific mAbs. By contrast, activation of Jurkat-NKG2C+ was undetectable upon interaction with Human Fetal Foreskin Fibroblasts (HFFF) infected with HCMV laboratory strains (i.e., AD169, Towne), regardless of their differential ability to preserve surface HLA-E expression. On the other hand, infection with two clinical isolates or with the endotheliotropic TB40/E strain triggered Jurkat-NKG2C+ activation; yet, this response was not inhibited by blocking mAbs and was independent of CD94/NKG2C expression. The results are discussed in the framework of previous observations supporting the hypothetical existence of specific ligand(s) for CD94/NKG2C in HCMV-infected cells. | - |
dc.format.extent | 12 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Frontiers Media | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.3389/fimmu.2017.01317 | - |
dc.relation.ispartof | Frontiers in Immunology, 2017, vol. 8 | - |
dc.relation.uri | https://doi.org/10.3389/fimmu.2017.01317 | - |
dc.rights | cc-by (c) Pupuleku, Aldi et al., 2017 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es | - |
dc.source | Articles publicats en revistes (Biomedicina) | - |
dc.subject.classification | Citomegalovirus | - |
dc.subject.classification | Citometria de fluxe | - |
dc.subject.other | Cytomegaloviruses | - |
dc.subject.other | Flow cytometry | - |
dc.title | Elusive role of the CD94/NKG2C NK cell receptor in the response to cytomegalovirus: novel experimental observations in a reporter cell system | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.identifier.idgrec | 677229 | - |
dc.date.updated | 2019-08-30T08:09:42Z | - |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/FP7/317013/EU//NATURIMMUN | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 29114247 | - |
Appears in Collections: | Articles publicats en revistes (Biomedicina) Articles publicats en revistes (IDIBAPS: Institut d'investigacions Biomèdiques August Pi i Sunyer) |
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File | Description | Size | Format | |
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677229.pdf | 2.12 MB | Adobe PDF | View/Open |
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