{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T12:56:33Z","timestamp":1791204993263,"version":"4.1.0"},"reference-count":24,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2001,12,21]],"date-time":"2001-12-21T00:00:00Z","timestamp":1008892800000},"content-version":"vor","delay-in-days":142,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2001,8]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p> <jats:italic>Brucella abortus<\/jats:italic> is an intracellular bacterial pathogen that causes chronic infections in humans and a number of agriculturally important species of animals. It has been shown that BALB\/c mice are more susceptible to infections with virulent strains of <jats:italic>Brucella abortus<\/jats:italic> than C57BL\/6 or C57BL\/10 strains. In experiments described here, gene knock\u2010out mice were utilized to elucidate some of the salient components of resistance. Resistant C57BL\/6 mice with gene deletions or disruptions in the interferon\u2010\u03b3 (IFN\u2010\u03b3), perforin or \u03b2<jats:sub>2<\/jats:sub>\u2010microglobulin genes had decreased abilities to control intracellular infections with <jats:italic>B. abortus<\/jats:italic> strain 2308 during the first week after infection. However, only the IFN\u2010\u03b3 knock\u2010out mice had a sustained inability to control infections and this resulted in death of the mice at approximately 6\u2003weeks post\u2010infection. These mice had a continual increase in the number of bacterial colony\u2010forming units (CFU) in their spleens until death. When BALB\/c mice with the disrupted IFN\u2010\u03b3 gene were infected they had more splenic CFU at one week post\u2010infection than control mice but the increase was not statistically significant and by 3\u2003weeks they did not have more CFU than control mice. Moreover, the number of splenic bacteria did not increase in the BALB\/c IFN\u2010\u03b3 knock\u2010out mice between 6 and 10\u00b75\u2003weeks, although they died at 10\u00b75\u2003weeks, the time by which normal BALB\/c mice were clearing the infection. Death in both strains of IFN\u2010\u03b3 gene disrupted mice coincided with symptoms of cachexia and macrophages comprised \u2265\u200a75% of the splenic leucocytes.<\/jats:p>","DOI":"10.1046\/j.1365-2567.2001.01258.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T02:29:06Z","timestamp":1047436146000},"page":"511-518","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":213,"title":["Interferon\u2010\u03b3 is crucial for surviving a <i>Brucella abortus<\/i> infection in both resistant C57BL\/6 and susceptible BALB\/c mice"],"prefix":"10.1111","volume":"103","author":[{"given":"Erin A.","family":"Murphy","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janaki","family":"Sathiyaseelan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle 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