{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,2]],"date-time":"2026-05-02T14:15:37Z","timestamp":1777731337884,"version":"3.51.4"},"reference-count":34,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2018,5,1]],"date-time":"2018-05-01T00:00:00Z","timestamp":1525132800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Innate Immun"],"published-print":{"date-parts":[[2018,5]]},"abstract":"<jats:p>\n                    Murine NK cell Ly49 receptors, functionally analogous to KIRs in humans recognize MHC class I molecules and play a key role in controlling NK cell function. We have previously shown that the paired activating Ly49s4 and inhibitory Ly49i4 receptors recognize undefined non-classical MHC-Ib ligands from the RT1-CE region in rats. Here, the RT1-CE16 gene of the RT1\n                    <jats:sup>d<\/jats:sup>\n                    haplotype was stably transfected into the mouse RAW macrophage cell line, termed RAW-CE16\n                    <jats:sup>d<\/jats:sup>\n                    cells. Combining RAW-CE16\n                    <jats:sup>d<\/jats:sup>\n                    cells with Ly49 expressing reporter cells demonstrated Ly49i4 and Ly49s4 specificity for CE16\n                    <jats:sup>d<\/jats:sup>\n                    . The Ly49s4\/i4:CE16\n                    <jats:sup>d<\/jats:sup>\n                    interaction was confirmed by specific MHC-I blocking monoclonal Abs. Further, we used our in\u00a0vitro model to study the effect of Listeria monocytogenes (LM) on CE16\n                    <jats:sup>d<\/jats:sup>\n                    after infection. LM infection and IFN-\u03b3 stimulation both led to enhanced CE16\n                    <jats:sup>d<\/jats:sup>\n                    expression on the surface of transfected RAW-CE16\n                    <jats:sup>d<\/jats:sup>\n                    cells. Interestingly, the reporter cells displayed increased response to LM-infected RAW-CE16\n                    <jats:sup>d<\/jats:sup>\n                    cells compared with IFN-\u03b3-treated RAW-CE16\n                    <jats:sup>d<\/jats:sup>\n                    cells, suggesting a fundamental difference between these stimuli in supporting enhanced Ly49 recognition of CE16\n                    <jats:sup>d<\/jats:sup>\n                    . Collectively, our data show that Ly49s4 and Ly49i4 recognize the non-classical RT1-CE16\n                    <jats:sup>d<\/jats:sup>\n                    molecule, which in turn is up-regulated during LM infection and thereby may contribute to NK-mediated responses against infected cells.\n                  <\/jats:p>","DOI":"10.1177\/1753425918759589","type":"journal-article","created":{"date-parts":[[2018,5,24]],"date-time":"2018-05-24T01:27:43Z","timestamp":1527125263000},"page":"252-261","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":2,"title":["<i>Listeria monocytogenes<\/i>\n                    infection enhances the interaction between rat non-classical MHC-Ib molecule and Ly49 receptors"],"prefix":"10.1177","volume":"24","author":[{"given":"Hamid","family":"Shegarfi","sequence":"first","affiliation":[{"name":"Atlantis Medical University College, Trondheimsveien 2, Oslo, Norway"},{"name":"Department of Anatomy, Institute of Basic Medical Sciences, University of Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kevin P","family":"Kane","sequence":"additional","affiliation":[{"name":"Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Janne","family":"Nestvold","sequence":"additional","affiliation":[{"name":"Department of Transplantation Medicine, Institute for Surgical Research, Oslo University Hospital, Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2018,5,23]]},"reference":[{"key":"bibr1-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1016\/j.mib.2013.11.007"},{"key":"bibr2-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1038\/nri1461"},{"key":"bibr3-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.1997.tb00989.x"},{"key":"bibr4-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.1997.tb01000.x"},{"key":"bibr5-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1038\/nri1863"},{"key":"bibr6-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.23.021704.115526"},{"key":"bibr7-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.24.021605.090700"},{"key":"bibr8-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0110039"},{"key":"bibr9-1753425918759589","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2014.00283"},{"key":"bibr10-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1007\/s002510100361"},{"key":"bibr11-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1101\/gr.1987704"},{"key":"bibr12-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200425429"},{"key":"bibr13-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1038\/nri2276"},{"key":"bibr14-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1111\/imr.12315"},{"issue":"1","key":"bibr15-1753425918759589","doi-asserted-by":"crossref","first-page":"95","DOI":"10.1177\/135965350501000107","volume":"10","author":"Nattermann J","year":"2005","journal-title":"Antivir Ther"},{"key":"bibr16-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1016\/S0952-7915(00)00112-6"},{"key":"bibr17-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1159\/000324143"},{"key":"bibr18-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.1010593"},{"key":"bibr19-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1002\/eji.201040651"},{"key":"bibr20-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-3083.2009.02292.x"},{"issue":"2","key":"bibr21-1753425918759589","doi-asserted-by":"crossref","first-page":"743","DOI":"10.4049\/jimmunol.162.2.743","volume":"162","author":"Leong LY","year":"1999","journal-title":"J Immunol"},{"key":"bibr22-1753425918759589","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.174.5.2702"},{"key":"bibr23-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0015579"},{"key":"bibr24-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M801526200"},{"key":"bibr25-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1521-4141(199909)29:09<2748::AID-IMMU2748>3.0.CO;2-C"},{"key":"bibr26-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80082-5"},{"key":"bibr27-1753425918759589","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1002809"},{"key":"bibr28-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0131308"},{"key":"bibr29-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1007\/s00251-014-0777-2"},{"key":"bibr30-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1126\/science.1070884"},{"key":"bibr31-1753425918759589","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1401386"},{"key":"bibr32-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830120313"},{"key":"bibr33-1753425918759589","doi-asserted-by":"publisher","DOI":"10.1002\/1521-4141(200207)32:7<2031::AID-IMMU2031>3.0.CO;2-H"},{"key":"bibr34-1753425918759589","doi-asserted-by":"crossref","unstructured":"Shegarfi H, Rolstad B, Kane KP, et al. Listeria monocytogenes infection differentially affects expression of ligands for NK cells and NK cell responses, depending on the cell type infected.\n                      J Leukoc Biol\n                      2018. 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