{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T12:14:14Z","timestamp":1793794454216,"version":"4.6.1"},"reference-count":65,"publisher":"National Academy of Sciences","issue":"36","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2011,9,6]]},"abstract":"<jats:p>\n                    During human CMV infection, there is a preferential expansion of natural killer (NK) cells expressing the activating CD94\u2013NKG2C receptor complex, implicating this receptor in the recognition of CMV-infected cells. We hypothesized that NK cells expanded in response to pathogens will be marked by expression of CD57, a carbohydrate antigen expressed on highly mature cells within the CD56\n                    <jats:sup>dim<\/jats:sup>\n                    CD16\n                    <jats:sup>+<\/jats:sup>\n                    NK cell compartment. Here we demonstrate the preferential expansion of a unique subset of NK cells coexpressing the activating CD94\u2013NKG2C receptor and CD57 in CMV\n                    <jats:sup>+<\/jats:sup>\n                    donors. These CD57\n                    <jats:sup>+<\/jats:sup>\n                    NKG2C\n                    <jats:sup>hi<\/jats:sup>\n                    NK cells degranulated in response to stimulation through their NKG2C receptor. Furthermore, CD57\n                    <jats:sup>+<\/jats:sup>\n                    NKG2C\n                    <jats:sup>hi<\/jats:sup>\n                    NK cells preferentially lack expression of the inhibitory NKG2A receptor and the inhibitory KIR3DL1 receptor in individuals expressing its HLA-Bw4 ligand. Moreover, in solid-organ transplant recipients with active CMV infection, the percentage of CD57\n                    <jats:sup>+<\/jats:sup>\n                    NKG2C\n                    <jats:sup>hi<\/jats:sup>\n                    NK cells in the total NK cell population preferentially increased. During acute CMV infection, the NKG2C\n                    <jats:sup>+<\/jats:sup>\n                    NK cells proliferated, became NKG2C\n                    <jats:sup>hi<\/jats:sup>\n                    , and finally acquired CD57. Thus, we propose that CD57 might provide a marker of \u201cmemory\u201d NK cells that have been expanded in response to infection.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1110900108","type":"journal-article","created":{"date-parts":[[2011,8,9]],"date-time":"2011-08-09T02:20:00Z","timestamp":1312856400000},"page":"14725-14732","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":815,"title":["Expansion of a unique CD57\n                    <sup>+<\/sup>\n                    NKG2C\n                    <sup>hi<\/sup>\n                    natural killer cell subset during acute human cytomegalovirus infection"],"prefix":"10.1073","volume":"108","author":[{"given":"Sandra","family":"Lopez-Verg\u00e8s","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology and Cancer Research Institute,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey M.","family":"Milush","sequence":"additional","affiliation":[{"name":"Division of Experimental Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian S.","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, University of California, San Francisco, CA 94143;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcelo J.","family":"Pando","sequence":"additional","affiliation":[{"name":"Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica","family":"Jarjoura","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology and Cancer Research Institute,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vanessa A.","family":"York","sequence":"additional","affiliation":[{"name":"Division of Experimental Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey P.","family":"Houchins","sequence":"additional","affiliation":[{"name":"R&amp;D Systems, Minneapolis, MN 55431;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steve","family":"Miller","sequence":"additional","affiliation":[{"name":"Departments of Laboratory Medicine and Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sang-Mo","family":"Kang","sequence":"additional","affiliation":[{"name":"Division of Transplant Surgery, University of California, San Francisco, CA 94143; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Phillip J.","family":"Norris","sequence":"additional","affiliation":[{"name":"Departments of Laboratory Medicine and Medicine and"},{"name":"Blood Systems Research Institute, San Francisco, CA 94118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas F.","family":"Nixon","sequence":"additional","affiliation":[{"name":"Division of Experimental Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lewis L.","family":"Lanier","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology and Cancer Research Institute,"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2011,8,8]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2007-09-077438"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri2276"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198906293202605"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1286-4579(02)00038-2"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpeds.2004.11.022"},{"key":"e_1_3_3_6_2","doi-asserted-by":"crossref","first-page":"4480","DOI":"10.4049\/jimmunol.136.12.4480","article-title":"The relationship of CD16 (Leu-11) and Leu-19 (NKH-1) antigen expression on human peripheral blood NK cells and cytotoxic T lymphocytes","volume":"136","author":"Lanier LL","year":"1986","unstructured":"LL Lanier, AM Le, CI Civin, MR Loken, JH Phillips, The relationship of CD16 (Leu-11) and Leu-19 (NKH-1) antigen expression on human peripheral blood NK cells and cytotoxic T lymphocytes. 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