{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T22:50:37Z","timestamp":1790895037210,"version":"4.1.0"},"reference-count":30,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,7,17]],"date-time":"2012-07-17T00:00:00Z","timestamp":1342483200000},"content-version":"vor","delay-in-days":16,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2012,7]]},"abstract":"<jats:p><jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>assa virus (<jats:styled-content style=\"fixed-case\">LASV<\/jats:styled-content>) and <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>opeia virus (<jats:styled-content style=\"fixed-case\">MOPV<\/jats:styled-content>) are closely related <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>renaviruses. <jats:styled-content style=\"fixed-case\">LASV<\/jats:styled-content> causes hemorrhagic fever, whereas <jats:styled-content style=\"fixed-case\">MOPV<\/jats:styled-content> is not pathogenic. Both viruses display tropism for <jats:styled-content style=\"fixed-case\">APC<\/jats:styled-content>s such as <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s and macrophages. During viral infections, <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells are involved in the clearance of infected cells and promote optimal immune responses by interacting with <jats:styled-content style=\"fixed-case\">APC<\/jats:styled-content>s. We used an in vitro model of human <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">APC<\/jats:styled-content> coculture to study the role of <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells and to characterize their interactions with <jats:styled-content style=\"fixed-case\">APC<\/jats:styled-content>s during <jats:styled-content style=\"fixed-case\">LASV<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">MOPV<\/jats:styled-content> infections. As expected, <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells alone were neither infected nor activated by <jats:styled-content style=\"fixed-case\">LASV<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">MOPV<\/jats:styled-content>, and infected <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s did not activate <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells. By contrast, <jats:styled-content style=\"fixed-case\">LASV<\/jats:styled-content>\u2010 and <jats:styled-content style=\"fixed-case\">MOPV<\/jats:styled-content>\u2010infected macrophages activated <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells, as shown by the upregulation of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>69, <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>p30, and <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>p44, the downregulation of <jats:styled-content style=\"fixed-case\">CXCR<\/jats:styled-content>3, and an increase in <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>\u2010cell proliferation. <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells acquired enhanced cytotoxicity, as illustrated by the increase in granzyme B (<jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>rz<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>) expression and killing of <jats:styled-content style=\"fixed-case\">K<\/jats:styled-content>562 targets, but did not produce <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3. Contact between <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells and infected macrophages and type I <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>s were essential for activation; however, <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells could not kill infected cells and control infection. Overall, these findings show that <jats:styled-content style=\"fixed-case\">MOPV<\/jats:styled-content>\u2010 as well as pathogenic <jats:styled-content style=\"fixed-case\">LASV<\/jats:styled-content>\u2010infected macrophages mediate <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>\u2010cell activation.<\/jats:p>","DOI":"10.1002\/eji.201142099","type":"journal-article","created":{"date-parts":[[2012,5,14]],"date-time":"2012-05-14T12:49:49Z","timestamp":1336999789000},"page":"1822-1832","source":"Crossref","is-referenced-by-count":27,"title":["<scp>NK<\/scp> cells are strongly activated by <scp>L<\/scp>assa and <scp>M<\/scp>opeia virus\u2010infected human macrophages in vitro but do not mediate virus suppression"],"prefix":"10.1002","volume":"42","author":[{"given":"Marion","family":"Russier","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"St\u00e9phanie","family":"Reynard","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"No\u00ebl","family":"Tordo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvain","family":"Baize","sequence":"additional","affiliation":[{"name":"Unit\u00e9 de Biologie des Infections Virales Emergentes Institut Pasteur  Lyon France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,7,17]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/155.3.437"},{"key":"e_1_2_7_3_1","first-page":"441","article-title":"Isolation of an arenavirus closely related to Lassa virus from \n                     Mastomys natalensis in south\u2010east Africa","volume":"55","author":"Wulff H.","year":"1977","journal-title":"Bull. 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