{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T09:03:31Z","timestamp":1790327011988,"version":"4.1.0"},"reference-count":55,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2007,2,1]],"date-time":"2007-02-01T00:00:00Z","timestamp":1170288000000},"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":[[2007,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Both peptidoglycan and muropeptides potently modulate inflammatory and innate immune responses. The secreted Listeria monocytogenes p60 autolysin digests peptidoglycan and promotes bacterial infection in vivo. Here, we report that p60 contributes to bacterial subversion of NK cell activation and innate IFN-\u03b3 production. L. monocytogenes deficient for p60 (\u0394p60) competed well for expansion in mice doubly deficient for IFNAR1 and IFN-\u03b3R1 or singly deficient for IFN-\u03b3R1, but not in wild-type, IFNAR1\u2212\/\u2212, or TLR2\u2212\/\u2212 mice. The restored competitiveness of p60-deficient bacteria suggested a specific role for p60 in bacterial subversion of IFN-\u03b3-mediated immune responses, since in vivo expansion of three other mutant L. monocytogenes strains (\u0394ActA, \u0394NamA, and \u0394PlcB) was not complemented in IFN-\u03b3R1\u2212\/\u2212 mice. Bacterial expression of p60 was not required to induce socs1, socs3, and il10 expression in infected mouse bone marrow macrophages but did correlate with enhanced production of IL-6, IL-12p70, and most strikingly IFN-\u03b3. The primary source of p60-dependent innate IFN-\u03b3 was NK cells, whereas bacterial p60 expression did not significantly alter innate IFN-\u03b3 production by T cells. The mechanism for p60-dependent NK cell stimulation was also indirect, given that treatment with purified p60 protein failed to directly activate NK cells for IFN-\u03b3 production. These data suggest that p60 may act on infected cells to indirectly enhance NK cell activation and increase innate IFN-\u03b3 production, which presumably promotes early bacterial expansion through its immunoregulatory effects on bystander cells. Thus, the simultaneous induction of IFN-\u03b3 production and factors that inhibit IFN-\u03b3 signaling may be a common strategy for misdirection of early antibacterial immunity.<\/jats:p>","DOI":"10.4049\/jimmunol.178.4.2407","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:02:49Z","timestamp":1397847769000},"page":"2407-2414","source":"Crossref","is-referenced-by-count":45,"title":["Expression of the p60 Autolysin Enhances NK Cell Activation and Is Required for\n                    <i>Listeria monocytogenes<\/i>\n                    Expansion in IFN-\u03b3-Responsive Mice"],"prefix":"10.1093","volume":"178","author":[{"given":"Jessica","family":"Humann","sequence":"first","affiliation":[{"name":"Denver Health Sciences Center, University of Colorado , Denver, CO 80206"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan","family":"Bjordahl","sequence":"additional","affiliation":[{"name":"Denver Health Sciences Center, University of Colorado , Denver, CO 80206"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl","family":"Andreasen","sequence":"additional","affiliation":[{"name":"Integrated Department of Immunology, National Jewish Medical and Research Center, University of Colorado , Denver, CO 80206"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laurel L","family":"Lenz","sequence":"additional","affiliation":[{"name":"Integrated Department of Immunology, National Jewish Medical and Research Center, University of Colorado , Denver, CO 80206"},{"name":"Denver Health Sciences Center, University of Colorado , Denver, CO 80206"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2007,2,15]]},"reference":[{"key":"2026012811302904800_R1","first-page":"879","volume-title":"Science","year":"2006"},{"key":"2026012811302904800_R2","first-page":"599","volume-title":"Annu. 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