{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T19:40:19Z","timestamp":1788378019634,"version":"build-2803163510"},"reference-count":40,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2014,3,1]],"date-time":"2014-03-01T00:00:00Z","timestamp":1393632000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2014,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Oropharyngeal candidiasis (OPC; thrush) is an opportunistic fungal infection caused by the commensal microbe\n            <jats:named-content content-type=\"genus-species\">Candida albicans<\/jats:named-content>\n            . Immunity to OPC is strongly dependent on CD4\n            <jats:sup>+<\/jats:sup>\n            T cells, particularly those of the Th17 subset. Interleukin-17 (IL-17) deficiency in mice or humans leads to chronic mucocutaneous candidiasis, but the specific downstream mechanisms of IL-17-mediated host defense remain unclear. Lipocalin 2 (Lcn2; 24p3; neutrophil gelatinase-associated lipocalin [NGAL]) is an antimicrobial host defense factor produced in response to inflammatory cytokines, particularly IL-17. Lcn2 plays a key role in preventing iron acquisition by bacteria that use catecholate-type siderophores, and lipocalin 2\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice are highly susceptible to infection by\n            <jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>\n            and\n            <jats:named-content content-type=\"genus-species\">Klebsiella pneumoniae<\/jats:named-content>\n            . The role of Lcn2 in mediating immunity to fungi is poorly defined. Accordingly, in this study, we evaluated the role of Lcn2 in immunity to oral infection with\n            <jats:named-content content-type=\"genus-species\">C. albicans<\/jats:named-content>\n            . Lcn2 is strongly upregulated following oral infection with\n            <jats:named-content content-type=\"genus-species\">C. albicans<\/jats:named-content>\n            , and its expression is almost entirely abrogated in mice with defective IL-17 signaling (IL-17RA\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            or Act1\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice). However, Lcn2\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice were completely resistant to OPC, comparably to wild-type (WT) mice. Moreover, Lcn2 deficiency mediated protection from OPC induced by steroid immunosuppression. Therefore, despite its potent regulation during\n            <jats:named-content content-type=\"genus-species\">C. albicans<\/jats:named-content>\n            infection, Lcn2 is not required for immunity to mucosal candidiasis.\n          <\/jats:p>","DOI":"10.1128\/iai.01389-13","type":"journal-article","created":{"date-parts":[[2013,12,17]],"date-time":"2013-12-17T03:16:28Z","timestamp":1387250188000},"page":"1030-1035","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":65,"title":["Interleukin-17-Induced Protein Lipocalin 2 Is Dispensable for Immunity to Oral Candidiasis"],"prefix":"10.1128","volume":"82","author":[{"given":"Maria Carolina","family":"Ferreira","sequence":"first","affiliation":[{"name":"Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA"},{"name":"Department of Clinical Pathology, Campinas State University, UNICAMP, SP, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natasha","family":"Whibley","sequence":"additional","affiliation":[{"name":"Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna J.","family":"Mamo","sequence":"additional","affiliation":[{"name":"Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich","family":"Siebenlist","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation, NIAID, National Institutes of Health, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yvonne R.","family":"Chan","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Allergy, and Critical Care Medicine, Department of 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