{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T11:33:13Z","timestamp":1791286393818,"version":"4.1.0"},"reference-count":35,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2002,10,1]],"date-time":"2002-10-01T00:00:00Z","timestamp":1033430400000},"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":[[2002,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Listeria monocytogenes (LM), a facultative intracellular Gram-positive bacterium, often causes lethal infection of the host. In this study we investigated the molecular mechanism underlying LM eradication in the early phase of infection. Upon infection with LM, both IL-12 and IL-18 were produced, and then they synergistically induced IFN-\u03b3 production, leading to normal LM clearance in the host. IFN-\u03b3 knockout (KO) mice were highly susceptible to LM infection. IL-12\/IL-18 double knockout mice were also highly susceptible. Their susceptibility was less than that of IFN-\u03b3 KO mice, but more than that of single IL-12 or IL-18 KO mice. Mice deficient in myeloid differentiation factor 88 (MyD88), an essential adaptor molecule used by signal transduction pathways of all members of the Toll-like receptor (TLR) family, showed an inability to produce IL-12 and IFN-\u03b3 following LM infection and were most susceptible to LM. Furthermore, MyD88-deficient, but not IFN-\u03b3-deficient, Kupffer cells could not produce TNF-\u03b1 in response to LM in vitro, indicating the importance of MyD88-dependent TNF-\u03b1 production for host defense. As TLR2 KO, but not TLR4 KO, mice showed partial impairment in their capacity to produce IL-12, IFN-\u03b3, and TNF-\u03b1, TLR2 activation partly contributed to the induction of IL-12-mediated IFN-\u03b3 production. These results indicated a critical role for TLRs\/MyD88-dependent IL-12\/TNF-\u03b1 production and for IL-12- and IL-18-mediated IFN-\u03b3 production in early phase clearance of LM.<\/jats:p>","DOI":"10.4049\/jimmunol.169.7.3863","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T19:18:01Z","timestamp":1398107881000},"page":"3863-3868","source":"Crossref","is-referenced-by-count":222,"title":["Critical Roles of Myeloid Differentiation Factor 88-Dependent Proinflammatory Cytokine Release in Early Phase Clearance of\n                    <i>Listeria monocytogenes<\/i>\n                    in Mice"],"prefix":"10.1093","volume":"169","author":[{"given":"Ekihiro","family":"Seki","sequence":"first","affiliation":[{"name":"First Department of Surgery, Hyogo College of Medicine , Nishinomiya ,","place":["Japan"]},{"name":"Core Research for Evolutional Science and Technology, Japan Science and Technology Corp. , Tokyo 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Technology, Japan Science and Technology Corp. , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keishi","family":"Adachi","sequence":"additional","affiliation":[{"name":"Department of Immunology and Medical Zoology, Hyogo College of Medicine , Nishinomiya ,","place":["Japan"]},{"name":"Core Research for Evolutional Science and Technology, Japan Science and Technology Corp. , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroki","family":"Nakano","sequence":"additional","affiliation":[{"name":"Department of Immunology and Medical Zoology, Hyogo College of Medicine , Nishinomiya ,","place":["Japan"]},{"name":"Core Research for Evolutional Science and Technology, Japan Science and Technology Corp. , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shizue","family":"Futatsugi-Yumikura","sequence":"additional","affiliation":[{"name":"Department of Immunology and 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