{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T06:29:49Z","timestamp":1791268189381,"version":"4.1.0"},"reference-count":71,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2013,2,5]],"date-time":"2013-02-05T00:00:00Z","timestamp":1360022400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-sa\/3.0\/"},{"start":{"date-parts":[[2013,3,1]],"date-time":"2013-03-01T00:00:00Z","timestamp":1362096000000},"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":["mBio"],"published-print":{"date-parts":[[2013,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    We assessed the role of Dectin-1 in the immune response to the pathogenic fungus\n                    <jats:italic>Coccidioides<\/jats:italic>\n                    , both\n                    <jats:italic>in vitro<\/jats:italic>\n                    and\n                    <jats:italic>in vivo<\/jats:italic>\n                    , using mice with a targeted mutation in\n                    <jats:italic>Clec7a<\/jats:italic>\n                    . Elicited peritoneal macrophages responded to formalin-killed spherules (FKS) and alkali-treated FKS by secreting proinflammatory cytokines in a Dectin-1- and \u03b2-glucan-dependent manner. The responses of bone marrow-derived dendritic cells (BMDC) to the same stimulants were more complex; interleukin 1\u03b2 (IL-1\u03b2) and tumor necrosis factor alpha (TNF-\u03b1) secretion was independent of Dectin-1, while IL-6, IL-10, and granulocyte-macrophage colony-stimulating factor (GM-CSF) were largely but not entirely dependent on Dectin-1. After intranasal infection, Dectin-1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice had lower concentrations of IL-12p70, gamma interferon (IFN-\u03b3), IL-1\u03b2, and the Th17 cytokines IL-22, IL-23, and 17A in the lung lavage fluid, which may explain why they were significantly more susceptible to pulmonary coccidioidomycosis two\u00a0weeks after infection. The Dectin-1 mutation was even more deleterious in (B6 \u00d7 DBA\/2)F\n                    <jats:sub>2<\/jats:sub>\n                    mice, which are more resistant to coccidioidomycosis than B6 mice by virtue of protective genes from DBA\/2, a genetically resistant strain. We also found that two susceptible strains of mice (B6 and BALB\/c) expressed much less Dectin-1 in their lungs than did resistant DBA\/2 mice. We conclude that Dectin-1 is necessary for resistance to\n                    <jats:italic>Coccidioides\u00a0immitis<\/jats:italic>\n                    , that Dectin-1 promotes both Th1 and Th17 protective immune responses to this infection, and that there is a correlation between expression of Dectin-1 by the inflammatory infiltrate and resistance to coccidioidomycosis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>IMPORTANCE<\/jats:bold>\n                    Coccidioidomycosis is a fungal infection endemic in the southwestern United States and neighboring Mexico, causing ~150,000 lung infections in people and resulting in ~17,000 hospitalizations annually in California alone. Very little is known about innate immunity to this fungus. This paper shows that Dectin-1, the primary \u03b2-glucan receptor on myeloid cells, is required for resistance to this pathogen. Dectin-1 is part of the innate immune system, and it is needed to direct the acquired immune response toward into a pathway that will lead to macrophage activation. Lungs from infected mice lacking Dectin-1 had lower concentrations of Th1 and Th17 cytokines, two cytokine pathways that are very important for acquired T cell immunity to\n                    <jats:italic>Coccidioides<\/jats:italic>\n                    spp. This is the first demonstration that Dectin-1 is required for host resistance to a dimorphic, primary pathogenic fungus.\n                  <\/jats:p>","DOI":"10.1128\/mbio.00597-12","type":"journal-article","created":{"date-parts":[[2013,2,5]],"date-time":"2013-02-05T21:25:15Z","timestamp":1360099515000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":66,"title":["Dectin-1 Is Required for Resistance to Coccidioidomycosis in Mice"],"prefix":"10.1128","volume":"4","author":[{"given":"Suganya","family":"Viriyakosol","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, University of California San Diego School of Medicine, San Diego, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria del Pilar","family":"Jimenez","sequence":"additional","affiliation":[{"name":"Departamento de Microbiolog\u00eda y Parasitolog\u00eda, Facultad de Medicina, Universidad de Antioquia, Medell\u00edn, Colombia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael A.","family":"Gurney","sequence":"additional","affiliation":[{"name":"Department of Microbiology, San Diego State University, San Diego, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark E.","family":"Ashbaugh","sequence":"additional","affiliation":[{"name":"Medical Service, VA Healthcare, San Diego, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua","family":"Fierer","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, University of California San Diego School of Medicine, San Diego, California, USA"},{"name":"Medical Service, VA Healthcare, San Diego, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pmed.0020002"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1080\/15572536.2003.11833250"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1086\/496991"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1080\/mmy.39.1.31.40"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.3201\/eid0203.960305"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.3.3.247"},{"key":"e_1_3_1_8_2","doi-asserted-by":"publisher","DOI":"10.1097\/00005792-197509000-00002"},{"key":"e_1_3_1_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(93)90054-S"},{"key":"e_1_3_1_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0923-2494(98)80765-7"},{"key":"e_1_3_1_11_2","article-title":"Role of IFN-gamma against coccidioides immitis infection, abstr. 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