{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T12:18:38Z","timestamp":1791289118401,"version":"4.3.0"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2008,5,1]],"date-time":"2008-05-01T00:00:00Z","timestamp":1209600000000},"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":[[2008,5,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Chemokine receptor-mediated recruitment of inflammatory cells is essential for innate immune defense against microbial infection. Recruitment of Ly6Chigh inflammatory monocytes from bone marrow to sites of microbial infection is dependent on CCR2, a chemokine receptor that responds to MCP-1 and MCP-3. Although CCR2\u2212\/\u2212 mice are markedly more susceptible to Listeria monocytogenes infection than are wild-type mice, MCP-1\u2212\/\u2212 mice have an intermediate phenotype, suggesting that other CCR2 ligands contribute to antimicrobial defense. Herein, we show that L. monocytogenes infection rapidly induces MCP-3 in tissue culture macrophages and in serum, spleen, liver, and kidney following in vivo infection. Only cytosol invasive L. monocytogenes induce MCP-3, suggesting that cytosolic innate immune detection mechanisms trigger chemokine production. MCP-3\u2212\/\u2212 mice clear bacteria less effectively from the spleen than do wild-type mice, a defect that correlates with diminished inflammatory monocyte recruitment. MCP-3\u2212\/\u2212 mice have significantly fewer Ly6Chigh monocytes in the spleen and bloodstream, and increased monocyte numbers in bone marrow. MCP-3\u2212\/\u2212 mice, like MCP-1\u2212\/\u2212 mice, have fewer TNF- and inducible NO synthase-producing dendritic cells (Tip-DCs) in the spleen following L. monocytogenes infection. Our data demonstrate that MCP-3 and MCP-1 provide parallel contributions to CCR2-mediated inflammatory monocyte recruitment and that both chemokines are required for optimal innate immune defense against L. monocytogenes infection.<\/jats:p>","DOI":"10.4049\/jimmunol.180.10.6846","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T18:52:44Z","timestamp":1397847164000},"page":"6846-6853","source":"Crossref","is-referenced-by-count":231,"title":["Additive Roles for MCP-1 and MCP-3 in CCR2-Mediated Recruitment of Inflammatory Monocytes during\n                    <i>Listeria monocytogenes<\/i>\n                    Infection"],"prefix":"10.1093","volume":"180","author":[{"given":"Ting","family":"Jia","sequence":"first","affiliation":[{"name":"Infectious Diseases Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center , New York, NY 10021"},{"name":"Program in Immunology and Microbial Pathogenesis, Weill Graduate School of Medical Sciences of Cornell University , New York, NY 10065"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalya V","family":"Serbina","sequence":"additional","affiliation":[{"name":"Infectious Diseases Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katharina","family":"Brandl","sequence":"additional","affiliation":[{"name":"Infectious Diseases Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maggie X","family":"Zhong","sequence":"additional","affiliation":[{"name":"Infectious Diseases Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ingrid M","family":"Leiner","sequence":"additional","affiliation":[{"name":"Infectious Diseases Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Israel F","family":"Charo","sequence":"additional","affiliation":[{"name":"Gladstone Institute of Cardiovascular Disease, University of California , San Francisco, CA 94158"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric G","family":"Pamer","sequence":"additional","affiliation":[{"name":"Infectious Diseases Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center , New York, NY 10021"},{"name":"Program in Immunology and Microbial Pathogenesis, Weill Graduate School of Medical Sciences of Cornell University , New York, NY 10065"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2008,5,15]]},"reference":[{"key":"2026012809121889300_R1","first-page":"891","volume-title":"Annu. 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