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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 | 2019-08-30T08:09:42Z |
dc.date | 2019-08-30T08:09:42Z |
dc.date | 2017-10-24 |
dc.date | 2019-08-30T08:09:42Z |
dc.identifier | 1664-3224 |
dc.identifier | 677229 |
dc.identifier | 29114247 |
dc.identifier.uri | http://hdl.handle.net/2445/138857 |
dc.description | 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 | 12 p. |
dc.format | application/pdf |
dc.language | eng |
dc.publisher | Frontiers Media |
dc.relation | Reproducció del document publicat a: https://doi.org/10.3389/fimmu.2017.01317 |
dc.relation | Frontiers in Immunology, 2017, vol. 8 |
dc.relation | https://doi.org/10.3389/fimmu.2017.01317 |
dc.relation | info:eu-repo/grantAgreement/EC/FP7/317013/EU//NATURIMMUN |
dc.rights | cc-by (c) Pupuleku, Aldi et al., 2017 |
dc.rights | http://creativecommons.org/licenses/by/3.0/es |
dc.rights | info:eu-repo/semantics/openAccess |
dc.subject | Citomegalovirus |
dc.subject | Citometria de fluxe |
dc.subject | Cytomegaloviruses |
dc.subject | 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 |