{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T06:45:13Z","timestamp":1787294713446,"version":"build-2736575974"},"reference-count":72,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2012,4,1]],"date-time":"2012-04-01T00:00:00Z","timestamp":1333238400000},"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":[[2012,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Previous research in our laboratory has demonstrated that repeated intranasal exposure to\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Aspergillus fumigatus<\/jats:named-content>\n                    conidia in C57BL\/6 mice results in a chronic pulmonary inflammatory response that reaches its maximal level after four challenges. The inflammatory response is characterized by eosinophilia, goblet cell metaplasia, and T helper T\n                    <jats:sub>H<\/jats:sub>\n                    2 cytokine production, which is accompanied by sustained interleukin-17 (IL-17) expression that persists even after the T\n                    <jats:sub>H<\/jats:sub>\n                    2 response has begun to resolve. T\n                    <jats:sub>H<\/jats:sub>\n                    17 cells could develop in mice deficient in gamma interferon (IFN-\u03b3), IL-4, or IL-10. In the lungs of IL-17 knockout mice repeatedly challenged with\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">A. fumigatus<\/jats:named-content>\n                    conidia, inflammation was attenuated (with the most significant decrease occurring in eosinophils), conidial clearance was enhanced, and the early transient peak of CD4\n                    <jats:sup>+<\/jats:sup>\n                    CD25\n                    <jats:sup>+<\/jats:sup>\n                    FoxP3\n                    <jats:sup>+<\/jats:sup>\n                    cells blunted. IL-17 appeared to play only a minor role in eosinophil differentiation in the bone marrow but a central role in eosinophil extravasation from the blood into the lungs. These observations point to an expanded role for IL-17 in driving T\n                    <jats:sub>H<\/jats:sub>\n                    2-type inflammation to repeated inhalation of fungal conidia.\n                  <\/jats:p>","DOI":"10.1128\/iai.05529-11","type":"journal-article","created":{"date-parts":[[2012,1,18]],"date-time":"2012-01-18T00:17:41Z","timestamp":1326845861000},"page":"1424-1436","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":83,"title":["Interleukin-17 Drives Pulmonary Eosinophilia following Repeated Exposure to Aspergillus fumigatus Conidia"],"prefix":"10.1128","volume":"80","author":[{"given":"Benjamin J.","family":"Murdock","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole 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