{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T03:34:52Z","timestamp":1770089692879,"version":"3.49.0"},"reference-count":58,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2003,9,1]],"date-time":"2003-09-01T00:00:00Z","timestamp":1062374400000},"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":[[2003,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Effects of adenoviral infection on in vivo responses to LPS mediated by TNF-\u03b1 were evaluated in a murine model. Adenovirus-infected mice showed decreased mortality from fulminant hepatitis induced by administration of LPS or staphylococcal enterotoxin B in the presence of D-galactosamine. Importantly, TNF-\u03b1 resistance genes within adenoviral E3 region were not required, because E1,E3-deleted vectors showed similar effects. Adenovirus-infected mice exhibited higher TNF-\u03b1 levels after LPS stimulation, no difference in TNFR1 expression, and similar mortality from Fas-induced fulminant hepatitis. Decreased production of IL-6 and KC in response to exogenous TNF-\u03b1, in addition to protection from TNF-\u03b1, suggested that adenoviral infection results in TNF-\u03b1 tolerance.<\/jats:p>","DOI":"10.4049\/jimmunol.171.5.2453","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T20:54:01Z","timestamp":1398027241000},"page":"2453-2460","source":"Crossref","is-referenced-by-count":4,"title":["Adenoviral Infection Decreases Mortality from Lipopolysaccharide-Induced Liver Failure Via Induction of TNF-\u03b1 Tolerance"],"prefix":"10.1093","volume":"171","author":[{"given":"Timur O","family":"Yarovinsky","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa and Veteran Affairs Medical Center , Iowa City, IA 52242"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Linda S","family":"Powers","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa and Veteran Affairs Medical Center , Iowa City, IA 52242"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Noah S","family":"Butler","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa and Veteran Affairs Medical Center , Iowa City, IA 52242"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mary A","family":"Bradford","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa and Veteran Affairs Medical Center , Iowa City, IA 52242"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martha M","family":"Monick","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa and Veteran Affairs Medical Center , Iowa City, IA 52242"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gary W","family":"Hunninghake","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa and Veteran Affairs Medical Center , Iowa City, IA 52242"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2003,9,1]]},"reference":[{"key":"2026020210201343500_R1","first-page":"1053","volume-title":"J. 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