{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T01:37:27Z","timestamp":1790818647921,"version":"4.1.0"},"reference-count":0,"publisher":"Rockefeller University Press","issue":"5","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1996,11,1]]},"abstract":"<jats:p>The activation of natural killer (NK) cells, cytotoxic lymphocytes capable of major histocompatibility complex (MHC)-unrestricted killing and early antiviral defense, is temporally related to the increased interferon (IFN)-alpha\/beta production that is seen in the viral infection of mice. Type I IFN (IFN-alpha\/beta) are expressed in many cell types early after primary viral infection and have been shown to mediate resistance against a variety of viruses. In this study, the role of the transcriptional activator IFN regulatory factor-1 (IRF-1) in murine NK cell activity was assessed. IRF-1-deficient mice displayed a normal frequency of NK marker-positive cells, but exhibited greatly reduced NK cell-mediated cytotoxicity after both virus infection and stimulation with the IFN inducer polyinosinic:polycytidilic acid in vivo. In vitro, cytolytic activity in IRF-1-deficient NK cells remained defective after stimulation with IFN-beta, IL-2, and IL-12. IRF-1-deficient mice were unable to eliminate syngeneic MHC class I-negative tumor cells in vivo, and had a reduced ability to reject parental semi-allogeneic donor cells from the circulation. Thus, IRF-1 is essential for the induction of NK cell-mediated cytotoxicity and for the in vivo effector functions that are mediated by this activity.<\/jats:p>","DOI":"10.1084\/jem.184.5.2043","type":"journal-article","created":{"date-parts":[[2004,6,24]],"date-time":"2004-06-24T07:56:10Z","timestamp":1088063770000},"page":"2043-2048","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":112,"title":["The transcription factor interferon regulatory factor-1 is essential for natural killer cell function in vivo."],"prefix":"10.1084","volume":"184","author":[{"given":"G S","family":"Duncan","sequence":"first","affiliation":[{"name":"Amgen Institute, Toronto, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H W","family":"Mittr\u00fccker","sequence":"additional","affiliation":[{"name":"Amgen Institute, Toronto, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D","family":"K\u00e4gi","sequence":"additional","affiliation":[{"name":"Amgen Institute, Toronto, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T","family":"Matsuyama","sequence":"additional","affiliation":[{"name":"Amgen Institute, Toronto, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T W","family":"Mak","sequence":"additional","affiliation":[{"name":"Amgen Institute, Toronto, Ontario, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[1996,11,1]]},"container-title":["The Journal of experimental medicine"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/rupress.org\/jem\/article-pdf\/184\/5\/2043\/1679522\/2043.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/rupress.org\/jem\/article-pdf\/184\/5\/2043\/1679522\/2043.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,25]],"date-time":"2023-07-25T07:28:19Z","timestamp":1690270099000},"score":1,"resource":{"primary":{"URL":"https:\/\/rupress.org\/jem\/article\/184\/5\/2043\/51086\/The-transcription-factor-interferon-regulatory"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1996,11,1]]}},"URL":"https:\/\/doi.org\/10.1084\/jem.184.5.2043","relation":{},"ISSN":["0022-1007","1540-9538"],"issn-type":[{"value":"0022-1007","type":"print"},{"value":"1540-9538","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,11,1]]}}}