{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T12:23:53Z","timestamp":1790857433498,"version":"4.1.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2003,10,1]],"date-time":"2003-10-01T00:00:00Z","timestamp":1064966400000},"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":[[2003,10,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>LFA-1 (CD11a\/CD18) plays a key role in various inflammatory responses. Here we show that the acquired immune response to Listeria monocytogenes is highly biased toward type 1 in the absence of LFA-1. At the early stage of listeriosis, numbers of IFN-\u03b3 producers in the liver and spleen of LFA-1\u2212\/\u2212 mice were markedly increased compared with heterozygous littermates and V\u03b114+NKT cell-deficient mice, and NK cells were major IFN-\u03b3 producers. Numbers of IL-12 producers were also markedly elevated in LFA-1\u2212\/\u2212 mice compared with heterozygous littermates, and endogenous IL-12 neutralization impaired IFN-\u03b3 production by NK cells. Granulocyte depletion diminished numbers of IL-12 producers and IFN-\u03b3-secreting NK cells in the liver of LFA-1\u2212\/\u2212 mice. Granulocytes from the liver of L. monocytogenes-infected LFA-1\u2212\/\u2212 mice were potent IL-12 producers. Thus, in the absence of LFA-1, granulocytes are a major source of IL-12 at the early stage of listeriosis. We assume that highly biased type 1 immune responses in LFA-1\u2212\/\u2212 mice are caused by increased levels of IL-12 from granulocytes and that granulocytes play a major role in IFN-\u03b3 secretion by NK cells. In conclusion, LFA-1 regulates type 1 immune responses by controlling prompt infiltration of IL-12-producing granulocytes into sites of inflammation.<\/jats:p>","DOI":"10.4049\/jimmunol.171.8.3970","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T00:53:23Z","timestamp":1398041603000},"page":"3970-3976","source":"Crossref","is-referenced-by-count":21,"title":["Highly Biased Type 1 Immune Responses in Mice Deficient in LFA-1 in <i>Listeria monocytogenes<\/i> Infection Are Caused by Elevated IL-12 Production by Granulocytes"],"prefix":"10.1093","volume":"171","author":[{"given":"Masashi","family":"Emoto","sequence":"first","affiliation":[{"name":"Department of Immunology, Max-Planck- Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mamiko","family":"Miyamoto","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck- Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshiko","family":"Emoto","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck- Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Izumi","family":"Yoshizawa","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck- Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Volker","family":"Brinkmann","sequence":"additional","affiliation":[{"name":"Central Support Unit Microscopy, Max-Planck- Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nico","family":"van Rooijen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Immunology, Faculty of Medicine, Vrije Universiteit , Amsterdam ,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan H E","family":"Kaufmann","sequence":"additional","affiliation":[{"name":"Department of Immunology, Max-Planck- Institute for Infection Biology , Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,10,15]]},"reference":[{"key":"2025032708333406500_R1","first-page":"827","volume-title":"Annu. 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