Inhibition of the NKp30 activating receptor by pp65 of human cytomegalovirus
Human cytomegalovirus, a chief pathogen in immunocompromised people, can persist in a healthy immunocompetent host throughout life without being eliminated by the immune system. Here we show that pp65, the main tegument protein of human cytomegalovirus, inhibited natural killer cell cytotoxicity by...
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| Veröffentlicht in: | Nature immunology 2005-05, Vol.6 (5), p.515-523 |
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| creator | Arnon, Tal I Achdout, Hagit Levi, Ofer Markel, Gal Saleh, Nivin Katz, Gil Gazit, Roi Gonen-Gross, Tsufit Hanna, Jacob Nahari, Efrat Porgador, Angel Honigman, Alik Plachter, Bodo Mevorach, Dror Wolf, Dana G Mandelboim, Ofer |
| description | Human cytomegalovirus, a chief pathogen in immunocompromised people, can persist in a healthy immunocompetent host throughout life without being eliminated by the immune system. Here we show that pp65, the main tegument protein of human cytomegalovirus, inhibited natural killer cell cytotoxicity by an interaction with the activating receptor NKp30. This interaction was direct and specific, leading to dissociation of the linked CD3ζ from NKp30 and, consequently, to reduced killing. Thus, pp65 is a ligand for the NKp30 receptor and demonstrates a unique mechanism by which an intracellular viral protein causes general suppression of natural killer cell cytotoxicity by specific interaction with an activating receptor. |
| doi_str_mv | 10.1038/ni1190 |
| format | Article |
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Here we show that pp65, the main tegument protein of human cytomegalovirus, inhibited natural killer cell cytotoxicity by an interaction with the activating receptor NKp30. This interaction was direct and specific, leading to dissociation of the linked CD3ζ from NKp30 and, consequently, to reduced killing. Thus, pp65 is a ligand for the NKp30 receptor and demonstrates a unique mechanism by which an intracellular viral protein causes general suppression of natural killer cell cytotoxicity by specific interaction with an activating receptor.</description><identifier>ISSN: 1529-2908</identifier><identifier>EISSN: 1529-2916</identifier><identifier>DOI: 10.1038/ni1190</identifier><identifier>PMID: 15821739</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Cells, Cultured ; Cytomegalovirus - physiology ; Cytotoxicity ; Cytotoxicity, Immunologic - drug effects ; Gene Expression Regulation ; Human cytomegalovirus ; Humans ; Immune system ; Immunoglobulin Fc Fragments - immunology ; Immunology ; Infectious Diseases ; Killer Cells, Natural - drug effects ; Killer Cells, Natural - immunology ; Killer Cells, Natural - metabolism ; Kinetics ; Membrane Glycoproteins - antagonists & inhibitors ; Membrane Glycoproteins - metabolism ; Mice ; Natural Cytotoxicity Triggering Receptor 3 ; Pathogens ; Phosphoproteins - metabolism ; Phosphoproteins - pharmacology ; Protein Binding ; Receptors, Cell Surface - antagonists & inhibitors ; Receptors, Cell Surface - metabolism ; Receptors, Immunologic - antagonists & inhibitors ; Receptors, Immunologic - metabolism ; Viral Matrix Proteins - metabolism ; Viral Matrix Proteins - pharmacology</subject><ispartof>Nature immunology, 2005-05, Vol.6 (5), p.515-523</ispartof><rights>Springer Nature America, Inc. 2005</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c534t-905020e56b989de0ef5a4779c81ed658d02a2cecbb2979cda0a0ea235e9b81bf3</citedby><cites>FETCH-LOGICAL-c534t-905020e56b989de0ef5a4779c81ed658d02a2cecbb2979cda0a0ea235e9b81bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ni1190$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ni1190$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15821739$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arnon, Tal I</creatorcontrib><creatorcontrib>Achdout, Hagit</creatorcontrib><creatorcontrib>Levi, Ofer</creatorcontrib><creatorcontrib>Markel, Gal</creatorcontrib><creatorcontrib>Saleh, Nivin</creatorcontrib><creatorcontrib>Katz, Gil</creatorcontrib><creatorcontrib>Gazit, Roi</creatorcontrib><creatorcontrib>Gonen-Gross, Tsufit</creatorcontrib><creatorcontrib>Hanna, Jacob</creatorcontrib><creatorcontrib>Nahari, Efrat</creatorcontrib><creatorcontrib>Porgador, Angel</creatorcontrib><creatorcontrib>Honigman, Alik</creatorcontrib><creatorcontrib>Plachter, Bodo</creatorcontrib><creatorcontrib>Mevorach, Dror</creatorcontrib><creatorcontrib>Wolf, Dana G</creatorcontrib><creatorcontrib>Mandelboim, Ofer</creatorcontrib><title>Inhibition of the NKp30 activating receptor by pp65 of human cytomegalovirus</title><title>Nature immunology</title><addtitle>Nat Immunol</addtitle><addtitle>Nat Immunol</addtitle><description>Human cytomegalovirus, a chief pathogen in immunocompromised people, can persist in a healthy immunocompetent host throughout life without being eliminated by the immune system. Here we show that pp65, the main tegument protein of human cytomegalovirus, inhibited natural killer cell cytotoxicity by an interaction with the activating receptor NKp30. This interaction was direct and specific, leading to dissociation of the linked CD3ζ from NKp30 and, consequently, to reduced killing. Thus, pp65 is a ligand for the NKp30 receptor and demonstrates a unique mechanism by which an intracellular viral protein causes general suppression of natural killer cell cytotoxicity by specific interaction with an activating receptor.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cells, Cultured</subject><subject>Cytomegalovirus - physiology</subject><subject>Cytotoxicity</subject><subject>Cytotoxicity, Immunologic - drug effects</subject><subject>Gene Expression Regulation</subject><subject>Human cytomegalovirus</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immunoglobulin Fc Fragments - immunology</subject><subject>Immunology</subject><subject>Infectious Diseases</subject><subject>Killer Cells, Natural - drug effects</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Kinetics</subject><subject>Membrane Glycoproteins - 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Academic</collection><jtitle>Nature immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arnon, Tal I</au><au>Achdout, Hagit</au><au>Levi, Ofer</au><au>Markel, Gal</au><au>Saleh, Nivin</au><au>Katz, Gil</au><au>Gazit, Roi</au><au>Gonen-Gross, Tsufit</au><au>Hanna, Jacob</au><au>Nahari, Efrat</au><au>Porgador, Angel</au><au>Honigman, Alik</au><au>Plachter, Bodo</au><au>Mevorach, Dror</au><au>Wolf, Dana G</au><au>Mandelboim, Ofer</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of the NKp30 activating receptor by pp65 of human cytomegalovirus</atitle><jtitle>Nature immunology</jtitle><stitle>Nat Immunol</stitle><addtitle>Nat Immunol</addtitle><date>2005-05-01</date><risdate>2005</risdate><volume>6</volume><issue>5</issue><spage>515</spage><epage>523</epage><pages>515-523</pages><issn>1529-2908</issn><eissn>1529-2916</eissn><abstract>Human cytomegalovirus, a chief pathogen in immunocompromised people, can persist in a healthy immunocompetent host throughout life without being eliminated by the immune system. Here we show that pp65, the main tegument protein of human cytomegalovirus, inhibited natural killer cell cytotoxicity by an interaction with the activating receptor NKp30. This interaction was direct and specific, leading to dissociation of the linked CD3ζ from NKp30 and, consequently, to reduced killing. Thus, pp65 is a ligand for the NKp30 receptor and demonstrates a unique mechanism by which an intracellular viral protein causes general suppression of natural killer cell cytotoxicity by specific interaction with an activating receptor.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>15821739</pmid><doi>10.1038/ni1190</doi><tpages>9</tpages></addata></record> |
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| ispartof | Nature immunology, 2005-05, Vol.6 (5), p.515-523 |
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| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature Journals Online |
| subjects | Animals Biomedical and Life Sciences Biomedicine Cells, Cultured Cytomegalovirus - physiology Cytotoxicity Cytotoxicity, Immunologic - drug effects Gene Expression Regulation Human cytomegalovirus Humans Immune system Immunoglobulin Fc Fragments - immunology Immunology Infectious Diseases Killer Cells, Natural - drug effects Killer Cells, Natural - immunology Killer Cells, Natural - metabolism Kinetics Membrane Glycoproteins - antagonists & inhibitors Membrane Glycoproteins - metabolism Mice Natural Cytotoxicity Triggering Receptor 3 Pathogens Phosphoproteins - metabolism Phosphoproteins - pharmacology Protein Binding Receptors, Cell Surface - antagonists & inhibitors Receptors, Cell Surface - metabolism Receptors, Immunologic - antagonists & inhibitors Receptors, Immunologic - metabolism Viral Matrix Proteins - metabolism Viral Matrix Proteins - pharmacology |
| title | Inhibition of the NKp30 activating receptor by pp65 of human cytomegalovirus |
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