{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T16:02:01Z","timestamp":1791302521690,"version":"4.1.0"},"reference-count":34,"publisher":"National Academy of Sciences","issue":"52","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2011,12,27]]},"abstract":"<jats:p>\n                    LPS-induced TNF-\u03b1 factor (LITAF) mediates cytokine expression in response to endotoxin challenge. Previously, we reported that macrophage-specific LITAF-deficient (macLITAF\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) mice exposed to LPS have a delayed onset in the serum levels of proinflammatory cytokines and prolonged persistence of anti-inflammatory cytokines, but only partial protection from endotoxic shock. We postulated that greater protection might be achieved if LITAF were deleted from all LITAF-producing cells, including macrophages. Using a Cre-loxP system, we engineered a tamoxifen-induced recombination mouse [tamLITAF(i)\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ] that resulted in whole-body LITAF deficiency. Our findings demonstrate that (\n                    <jats:italic>i<\/jats:italic>\n                    ) tamLITAF(i)\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice are more resistant to systemic\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    LPS-induced lethality than our previous macLITAF\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, providing evidence that LITAF-producing cells other than LysMCre-positive cells play an important role in mediating endotoxic shock; (\n                    <jats:italic>ii<\/jats:italic>\n                    ) tamLITAF(i)\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice show a similar pattern of cytokine expression with decreased proinflammatory and prolonged anti-inflammatory mediators compared with WT mice; and (\n                    <jats:italic>iii<\/jats:italic>\n                    ) tamLITAF(i)\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, compared with WT mice, display a significant reduction in bone resorption and inflammation associated with a local chronic inflammatory disease\u2014namely, collagen antibody-induced arthritis. Our findings offer a unique model to study the role of LITAF in systemic and chronic local inflammatory processes, and pave the way for anti-LITAF therapeutic approaches for the treatment of TNF-mediated inflammatory diseases.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1111492108","type":"journal-article","created":{"date-parts":[[2011,12,13]],"date-time":"2011-12-13T00:15:49Z","timestamp":1323735349000},"page":"21247-21252","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":55,"title":["Whole-body deletion of LPS-induced TNF-\u03b1 factor (LITAF) markedly improves experimental endotoxic shock and inflammatory arthritis"],"prefix":"10.1073","volume":"108","author":[{"given":"Jamie C.","family":"Merrill","sequence":"first","affiliation":[{"name":"Center for Anti-Inflammatory Therapeutics, Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine, Boston, MA 02118; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"You","sequence":"additional","affiliation":[{"name":"Center for Anti-Inflammatory Therapeutics, Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine, Boston, MA 02118; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cara","family":"Constable","sequence":"additional","affiliation":[{"name":"Center for Anti-Inflammatory Therapeutics, Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine, Boston, MA 02118; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan E.","family":"Leeman","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Salomon","family":"Amar","sequence":"additional","affiliation":[{"name":"Center for Anti-Inflammatory Therapeutics, Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine, Boston, MA 02118; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2011,12,12]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.2006.03261.x"},{"key":"e_1_3_3_2_2","first-page":"48","article-title":"Studies on inflammation and wound healing: Angiogenesis and collagen synthesis stimulated in vivo by resident and activated wound macrophages","volume":"96","author":"Hunt TK","year":"1984","unstructured":"TK Hunt, DR Knighton, KK Thakral, WH Goodson, WS Andrews, Studies on inflammation and wound healing: Angiogenesis and collagen synthesis stimulated in vivo by resident and activated wound macrophages. 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