{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,18]],"date-time":"2026-10-18T10:17:22Z","timestamp":1792318642647,"version":"4.4.0"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2000,3,1]],"date-time":"2000-03-01T00:00:00Z","timestamp":951868800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2000,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>IL-18 induces IFN-\u03b3 and NK cell cytotoxicity, making it a logical target for viral antagonism of host defense. We demonstrate that the ectromelia poxvirus p13 protein, bearing homology to the mammalian IL-18 binding protein, binds IL-18, and inhibits its activity in vitro. Binding of IL-18 to the viral p13 protein was compared with binding to the cellular IL-18R. The dissociation constant of p13 for murine IL-18 is 5 nM, compared with 0.2 nM for the cellular receptor heterodimer. Mice infected with a p13 deletion mutant of ectromelia virus had elevated cytotoxicity for YAC-1 tumor cell targets compared with control animals. Additionally, the p13 deletion mutant virus exhibited decreased levels of infectivity. Our data suggest that inactivation of IL-18, and subsequent impairment of NK cell cytotoxicity, may be one mechanism by which ectromelia evades the host immune response.<\/jats:p>","DOI":"10.4049\/jimmunol.164.6.3246","type":"journal-article","created":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T16:28:33Z","timestamp":1398184113000},"page":"3246-3254","source":"Crossref","is-referenced-by-count":146,"title":["A Poxvirus Protein That Binds to and Inactivates IL-18, and Inhibits NK Cell Response"],"prefix":"10.1093","volume":"164","author":[{"given":"Teresa L","family":"Born","sequence":"first","affiliation":[{"name":"Immunex Corporation , Seattle WA 98101"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lynda A","family":"Morrison","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Saint Louis University , St. Louis, MO 63104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David J","family":"Esteban","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Saint Louis University , St. Louis, MO 63104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tim","family":"VandenBos","sequence":"additional","affiliation":[{"name":"Immunex Corporation , Seattle WA 98101"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lydia G","family":"Thebeau","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Saint Louis University , St. Louis, MO 63104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nanhai","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Saint Louis University , St. Louis, MO 63104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melanie K","family":"Spriggs","sequence":"additional","affiliation":[{"name":"Immunex Corporation , Seattle WA 98101"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John E","family":"Sims","sequence":"additional","affiliation":[{"name":"Immunex Corporation , Seattle WA 98101"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R Mark L","family":"Buller","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Saint Louis University , St. Louis, MO 63104"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2000,3,15]]},"reference":[{"key":"2026020213194952600_R1","first-page":"281","volume-title":"Adv. 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