Elucidating the mechanisms of influenza virus recognition by Ncr1
Natural killer (NK) cells are innate cytotoxic lymphocytes that specialize in the defense against viral infection and oncogenic transformation. Their action is tightly regulated by signals derived from inhibitory and activating receptors; the later include proteins such as the Natural Cytotoxicity R...
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| creator | Glasner, Ariella Zurunic, Antonija Meningher, Tal Lenac Rovis, Tihana Tsukerman, Pinchas Bar-On, Yotam Yamin, Rachel Meyers, Adrienne F A Mandeboim, Michal Jonjic, Stipan Mandelboim, Ofer |
| description | Natural killer (NK) cells are innate cytotoxic lymphocytes that specialize in the defense against viral infection and oncogenic transformation. Their action is tightly regulated by signals derived from inhibitory and activating receptors; the later include proteins such as the Natural Cytotoxicity Receptors (NCRs: NKp46, NKp44 and NKp30). Among the NCRs, NKp46 is the only receptor that has a mouse orthologue named Ncr1. NKp46/Ncr1 is also a unique marker expressed on NK and on Lymphoid tissue inducer (LTI) cells and it was implicated in the control of various viral infections, cancer and diabetes. We have previously shown that human NKp46 recognizes viral hemagglutinin (HA) in a sialic acid-dependent manner and that the O-glycosylation is essential for the NKp46 binding to viral HA. Here we studied the molecular interactions between Ncr1 and influenza viruses. We show that Ncr1 recognizes influenza virus in a sialic acid dependent manner and that N-glycosylation is important for this binding. Surprisingly we demonstrate that none of the predicted N-glycosilated residues of Ncr1 are essential for its binding to influenza virus and we thus conclude that other, yet unidentified N-glycosilated residues are responsible for its recognition. We have demonstrated that N glycosylation play little role in the recognition of mouse tumor cell lines and also showed the in-vivo importance of Ncr1 in the control of influenza virus infection by infecting C57BL/6 and BALB/c mice knockout for Ncr1 with influenza. |
| doi_str_mv | 10.1371/journal.pone.0036837 |
| format | Article |
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Their action is tightly regulated by signals derived from inhibitory and activating receptors; the later include proteins such as the Natural Cytotoxicity Receptors (NCRs: NKp46, NKp44 and NKp30). Among the NCRs, NKp46 is the only receptor that has a mouse orthologue named Ncr1. NKp46/Ncr1 is also a unique marker expressed on NK and on Lymphoid tissue inducer (LTI) cells and it was implicated in the control of various viral infections, cancer and diabetes. We have previously shown that human NKp46 recognizes viral hemagglutinin (HA) in a sialic acid-dependent manner and that the O-glycosylation is essential for the NKp46 binding to viral HA. Here we studied the molecular interactions between Ncr1 and influenza viruses. We show that Ncr1 recognizes influenza virus in a sialic acid dependent manner and that N-glycosylation is important for this binding. Surprisingly we demonstrate that none of the predicted N-glycosilated residues of Ncr1 are essential for its binding to influenza virus and we thus conclude that other, yet unidentified N-glycosilated residues are responsible for its recognition. We have demonstrated that N glycosylation play little role in the recognition of mouse tumor cell lines and also showed the in-vivo importance of Ncr1 in the control of influenza virus infection by infecting C57BL/6 and BALB/c mice knockout for Ncr1 with influenza.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0036837</identifier><identifier>PMID: 22615821</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acids ; Animals ; Antigens, Ly - physiology ; Base Sequence ; Binding ; Biocompatibility ; Biology ; Cancer ; Cytotoxicity ; Diabetes mellitus ; Diabetes therapy ; DNA Primers ; Flow Cytometry ; Fusobacterium nucleatum ; Glycosylation ; Health aspects ; Hemagglutinins ; House mouse ; Infection control ; Infections ; Influenza ; Influenza viruses ; Laboratories ; Lectins ; Leishmania major ; Lymphocytes ; Lymphoid tissue ; Mice ; Molecular interactions ; Natural Cytotoxicity Triggering Receptor 1 - physiology ; Natural killer cells ; Organic acids ; Orthomyxoviridae - physiology ; Polymerase Chain Reaction ; Proteins ; Receptors ; Recognition ; Residues ; Rodents ; T cell receptors ; Toxicity ; Transformation ; Tumor cell lines ; Viruses</subject><ispartof>PloS one, 2012-05, Vol.7 (5), p.e36837-e36837</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Glasner et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Surprisingly we demonstrate that none of the predicted N-glycosilated residues of Ncr1 are essential for its binding to influenza virus and we thus conclude that other, yet unidentified N-glycosilated residues are responsible for its recognition. We have demonstrated that N glycosylation play little role in the recognition of mouse tumor cell lines and also showed the in-vivo importance of Ncr1 in the control of influenza virus infection by infecting C57BL/6 and BALB/c mice knockout for Ncr1 with influenza.</description><subject>Acids</subject><subject>Animals</subject><subject>Antigens, Ly - physiology</subject><subject>Base Sequence</subject><subject>Binding</subject><subject>Biocompatibility</subject><subject>Biology</subject><subject>Cancer</subject><subject>Cytotoxicity</subject><subject>Diabetes mellitus</subject><subject>Diabetes therapy</subject><subject>DNA Primers</subject><subject>Flow Cytometry</subject><subject>Fusobacterium nucleatum</subject><subject>Glycosylation</subject><subject>Health aspects</subject><subject>Hemagglutinins</subject><subject>House mouse</subject><subject>Infection control</subject><subject>Infections</subject><subject>Influenza</subject><subject>Influenza viruses</subject><subject>Laboratories</subject><subject>Lectins</subject><subject>Leishmania major</subject><subject>Lymphocytes</subject><subject>Lymphoid tissue</subject><subject>Mice</subject><subject>Molecular interactions</subject><subject>Natural Cytotoxicity Triggering Receptor 1 - physiology</subject><subject>Natural killer cells</subject><subject>Organic acids</subject><subject>Orthomyxoviridae - physiology</subject><subject>Polymerase Chain Reaction</subject><subject>Proteins</subject><subject>Receptors</subject><subject>Recognition</subject><subject>Residues</subject><subject>Rodents</subject><subject>T cell receptors</subject><subject>Toxicity</subject><subject>Transformation</subject><subject>Tumor cell lines</subject><subject>Viruses</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLgujFjPlqmt4Iw7LqwOKCLt6G0zTtZEiTMWkX119vxukuU9kLyUWSk-e8Jyd5s-wlRktMS_xh68fgwC533uklQpQLWj7KTnFFyYITRB8frU-yZzFuESqo4PxpdkIIx4Ug-DRbXdhRmQYG47p82Oi812oDzsQ-5r7NjWvtqN1vyG9MGGMetPKdM4PxLq9v868q4OfZkxZs1C-m-Sy7_nRxff5lcXn1eX2-ulwoXpFhQRiwSlSIAqm5wLhFTV1BmXalYFijWoumaoFWiBSEi9SQEkwV0GoERY3oWfb6ILuzPsqp-SgxZYwSTIsyEesD0XjYyl0wPYRb6cHIvwEfOglhMMpq2ShaU8YxwUywGreCElCpEFSctIWuk9bHqdpY97pR2g0B7Ex0fuLMRnb-RlJakIrSJPBuEgj-56jjIHsTlbYWnPZjujfCBeMlJzyhb_5BH-5uojpIDaR_8amu2ovKFStLJCiu9tTyASqNRvdGJae0JsVnCe9nCYkZ9K-hgzFGuf7-7f_Zqx9z9u0Ru9Fgh030dtw7J85BdgBV8DEG3d4_MkZyb_S715B7o8vJ6Cnt1fEH3SfdOZv-AbPb9tM</recordid><startdate>20120515</startdate><enddate>20120515</enddate><creator>Glasner, Ariella</creator><creator>Zurunic, Antonija</creator><creator>Meningher, Tal</creator><creator>Lenac Rovis, Tihana</creator><creator>Tsukerman, Pinchas</creator><creator>Bar-On, Yotam</creator><creator>Yamin, Rachel</creator><creator>Meyers, Adrienne F A</creator><creator>Mandeboim, Michal</creator><creator>Jonjic, Stipan</creator><creator>Mandelboim, Ofer</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120515</creationdate><title>Elucidating the mechanisms of influenza virus recognition by Ncr1</title><author>Glasner, Ariella ; Zurunic, Antonija ; Meningher, Tal ; Lenac Rovis, Tihana ; Tsukerman, Pinchas ; Bar-On, Yotam ; Yamin, Rachel ; Meyers, Adrienne F A ; Mandeboim, Michal ; Jonjic, Stipan ; Mandelboim, Ofer</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-24a498903a2b6811f0db9a7a2b7841e0be8d9fa39025268003c84c5afe0a5b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acids</topic><topic>Animals</topic><topic>Antigens, Ly - 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Their action is tightly regulated by signals derived from inhibitory and activating receptors; the later include proteins such as the Natural Cytotoxicity Receptors (NCRs: NKp46, NKp44 and NKp30). Among the NCRs, NKp46 is the only receptor that has a mouse orthologue named Ncr1. NKp46/Ncr1 is also a unique marker expressed on NK and on Lymphoid tissue inducer (LTI) cells and it was implicated in the control of various viral infections, cancer and diabetes. We have previously shown that human NKp46 recognizes viral hemagglutinin (HA) in a sialic acid-dependent manner and that the O-glycosylation is essential for the NKp46 binding to viral HA. Here we studied the molecular interactions between Ncr1 and influenza viruses. We show that Ncr1 recognizes influenza virus in a sialic acid dependent manner and that N-glycosylation is important for this binding. Surprisingly we demonstrate that none of the predicted N-glycosilated residues of Ncr1 are essential for its binding to influenza virus and we thus conclude that other, yet unidentified N-glycosilated residues are responsible for its recognition. We have demonstrated that N glycosylation play little role in the recognition of mouse tumor cell lines and also showed the in-vivo importance of Ncr1 in the control of influenza virus infection by infecting C57BL/6 and BALB/c mice knockout for Ncr1 with influenza.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22615821</pmid><doi>10.1371/journal.pone.0036837</doi><tpages>e36837</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Acids Animals Antigens, Ly - physiology Base Sequence Binding Biocompatibility Biology Cancer Cytotoxicity Diabetes mellitus Diabetes therapy DNA Primers Flow Cytometry Fusobacterium nucleatum Glycosylation Health aspects Hemagglutinins House mouse Infection control Infections Influenza Influenza viruses Laboratories Lectins Leishmania major Lymphocytes Lymphoid tissue Mice Molecular interactions Natural Cytotoxicity Triggering Receptor 1 - physiology Natural killer cells Organic acids Orthomyxoviridae - physiology Polymerase Chain Reaction Proteins Receptors Recognition Residues Rodents T cell receptors Toxicity Transformation Tumor cell lines Viruses |
| title | Elucidating the mechanisms of influenza virus recognition by Ncr1 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T23%3A01%3A15IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Elucidating%20the%20mechanisms%20of%20influenza%20virus%20recognition%20by%20Ncr1&rft.jtitle=PloS%20one&rft.au=Glasner,%20Ariella&rft.date=2012-05-15&rft.volume=7&rft.issue=5&rft.spage=e36837&rft.epage=e36837&rft.pages=e36837-e36837&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0036837&rft_dat=%3Cgale_plos_%3EA477083197%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1344321357&rft_id=info:pmid/22615821&rft_galeid=A477083197&rft_doaj_id=oai_doaj_org_article_dc3b346121484b1f832ace0aa962f5eb&rfr_iscdi=true |