{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T23:49:21Z","timestamp":1791071361257,"version":"4.1.0"},"reference-count":41,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2010,12,1]],"date-time":"2010-12-01T00:00:00Z","timestamp":1291161600000},"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":[[2010,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Cryptococcus neoformans<\/jats:italic>is an opportunistic fungal pathogen that causes disease in individuals with suppressed cell-mediated immunity. Recent studies in our laboratory have shown that increases in pulmonary Th1-type and interleukin-17A (IL-17A) cytokine production, classical macrophage activation, and sterilizing immunity are elicited in response to infection with a gamma interferon (IFN-\u03b3)-producing<jats:italic>C. neoformans<\/jats:italic>strain, H99\u03b3. IL-17A-treated macrophages, compared to IL-4-treated macrophages, have been demonstrated to exhibit increased microbicidal activity<jats:italic>in vitro<\/jats:italic>, a characteristic consistent with classical macrophage activation. The purpose of these studies is to determine the role of IL-17A in the induction of classically activated macrophages following infection with<jats:italic>C. neoformans<\/jats:italic>. Immunohistochemistry and real-time PCR were used to characterize the macrophage activation phenotype in lung tissues of mice treated with isotype control or anti-IL-17A antibodies and given an experimental pulmonary infection with<jats:italic>C. neoformans<\/jats:italic>strain H99\u03b3. The pulmonary fungal burden was resolved, albeit more slowly, in mice depleted of IL-17A compared to the fungal burden in isotype control-treated mice. Nonetheless, no difference in classical macrophage activation was observed in IL-17A-depleted mice. Similarly, classical macrophage activation was evident in mice deficient in IL-17A or the IL-17 receptor A, which mediates IL-17A signaling, following pulmonary infection with wild-type<jats:italic>C. neoformans<\/jats:italic>strain H99 or H99\u03b3. These studies suggest that IL-17A may play a role in the early immune response to<jats:italic>C. neoformans<\/jats:italic>but is not required for classical macrophage activation in mice experimentally infected with<jats:italic>C. neoformans<\/jats:italic>.<\/jats:p>","DOI":"10.1128\/iai.00845-10","type":"journal-article","created":{"date-parts":[[2010,10,5]],"date-time":"2010-10-05T03:20:04Z","timestamp":1286248804000},"page":"5341-5351","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":56,"title":["Interleukin-17 Is Not Required for Classical Macrophage Activation in a Pulmonary Mouse Model of<i>Cryptococcus neoformans<\/i>Infection"],"prefix":"10.1128","volume":"78","author":[{"given":"Sarah E.","family":"Hardison","sequence":"first","affiliation":[{"name":"Department of Biology"},{"name":"South Texas Center for Emerging Infectious Diseases, University of Texas at San Antonio, San Antonio, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen L.","family":"Wozniak","sequence":"additional","affiliation":[{"name":"Department of Biology"},{"name":"South Texas Center for Emerging Infectious Diseases, University of Texas at San Antonio, San Antonio, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay K.","family":"Kolls","sequence":"additional","affiliation":[{"name":"Louisiana State University Health Sciences Center, New Orleans, Lousiana"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"Floyd L.","family":"Wormley","sequence":"additional","affiliation":[{"name":"Department of Biology"},{"name":"South Texas Center for Emerging Infectious Diseases, University of Texas at San Antonio, San Antonio, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1007\/s004390000399"},{"key":"e_1_3_2_3_2","first-page":"164","volume":"84","year":"1976","unstructured":"Adams, D. 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