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Despite its medical importance, the immune responses required to control infection, including the role of interleukin-17 (IL-17), which is important in controlling other fungal infections, have not been clearly defined. Using flow cytometry and intracellular cytokine staining after stimulation with phorbol myristate acetate and ionomycin, we examined gamma interferon (IFN-\u03b3), IL-4, IL-5, and IL-17 production by lung lymphocytes in immunocompetent C57BL\/6 mice over time following infection with<jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content><jats:italic>murina<\/jats:italic>. We also examined the clearance of<jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>infection in IL-17A-deficient mice. The production of both IFN-\u03b3 and IL-17 by pulmonary lymphocytes increased during infection, with maximum production at approximately days 35 to 40, coinciding with peak<jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>levels in the lungs, while minimal changes were seen in IL-4- and IL-5-positive cells. The proportion of cells producing IFN-\u03b3 was consistently higher than for cells producing IL-17, with peak levels of \u223c25 to 30% of CD3<jats:sup>+<\/jats:sup>T cells for the former compared to \u223c15% for the latter. Both CD4<jats:sup>+<\/jats:sup>T cells and \u03b3\u03b4 T cells produced IL-17. Administration of anti-IFN-\u03b3 antibody led to a decrease in IFN-\u03b3-positive cells, and an increase in IL-5-positive cells, but did not impact clearance of<jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>infection. Despite the increases in IL-17 production during infection, IL-17A-deficient mice cleared<jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>infection with kinetics similar to C57BL\/6 mice. Thus, while IL-17 production in the lungs is increased during<jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>infection in immunocompetent mice, IL-17A is not required for control of<jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>infection.<\/jats:p>","DOI":"10.1128\/iai.00434-16","type":"journal-article","created":{"date-parts":[[2017,4,25]],"date-time":"2017-04-25T00:25:27Z","timestamp":1493079927000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":18,"title":["Pulmonary Interleukin-17-Positive Lymphocytes Increase during Pneumocystis murina Infection but Are Not Required for Clearance of Pneumocystis"],"prefix":"10.1128","volume":"85","author":[{"given":"Chiara","family":"Ripamonti","sequence":"first","affiliation":[{"name":"Critical Care Medicine Department, NIH Clinical Center, National Institutes of Health, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa R.","family":"Bishop","sequence":"additional","affiliation":[{"name":"Critical Care Medicine Department, NIH Clinical Center, National Institutes of Health, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5191-9880","authenticated-orcid":false,"given":"Joseph A.","family":"Kovacs","sequence":"additional","affiliation":[{"name":"Critical Care Medicine Department, NIH Clinical Center, National Institutes of Health, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb\/5.2.186"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.172.3.937"},{"key":"e_1_3_2_4_2","first-page":"1173","article-title":"Spontaneous Pneumocystis carinii pneumonia in immunodeficient mutant scid mice: natural history and pathobiology","volume":"136","author":"Roths JB","year":"1990","unstructured":"Roths JB Marshall JD Allen RD Carlson GA Sidman CL . 1990. 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