{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,2]],"date-time":"2026-05-02T14:14:54Z","timestamp":1777731294521,"version":"3.51.4"},"reference-count":46,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2013,5,30]],"date-time":"2013-05-30T00:00:00Z","timestamp":1369872000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Innate Immun"],"published-print":{"date-parts":[[2014,2]]},"abstract":"<jats:p>We have previously reported that the co-culture of functional T-cell hybridoma B6HO3 with dying J774 macrophage cells infected with Listeria monocytogenes (LM) results in the production of IFN-\u03b3 by B6HO3 cells. Here, we explore the mechanism underlying this phenomenon. We found that IFN-\u03b3 production was dependent on IL-18, but that the dying LM-infected macrophages produced no more than 100\u2009pg\/ml of IL-18, much less than the amount of IL-18 required for stimulating B6HO3 cells to produce IFN-\u03b3. Furthermore, IL-18 binding protein added to the co-culture was unable to easily gain access to IL-18 for neutralisation. B6HO3 cells formed cell conjugates with J774 macrophages, and IFN-\u03b3-producing B6HO3 cells were spatially and temporally associated with LM-infected macrophage cell death that exhibited neither pyroptosis nor pyronecrosis. These results suggest that the IL-18 produced by dying LM-infected macrophages is released to the interface of the cell conjugates, thereby inducing B6HO3 cells to produce IFN-\u03b3. Based on the present and also previous findings, we propose that IL-18 released from macrophages because of cell death caused by bacteria may be the primary cytokine that triggers the innate IFN-\u03b3 production that is required for activating the bactericidal functions of macrophages at early stages of bacterial infection.<\/jats:p>","DOI":"10.1177\/1753425913485474","type":"journal-article","created":{"date-parts":[[2013,5,31]],"date-time":"2013-05-31T01:54:53Z","timestamp":1369965293000},"page":"133-144","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["IL-18 provided in dying bacterial-infected macrophages induces IFN-\u03b3 production in functional T-cell hybridoma B6HO3 through cell conjugates"],"prefix":"10.1177","volume":"20","author":[{"given":"Koichi","family":"Kubota","sequence":"first","affiliation":[{"name":"Department of Microbiology, Kitasato University School of Medicine, Sagamihara, 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