{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T07:09:37Z","timestamp":1793171377410,"version":"4.5.0"},"reference-count":62,"publisher":"American Society for Clinical Investigation","issue":"22","license":[{"start":{"date-parts":[[2022,11,22]],"date-time":"2022-11-22T00:00:00Z","timestamp":1669075200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"crossref","award":["na"],"award-info":[{"award-number":["na"]}],"id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"crossref","award":["R01AI132140,R21AI152394,U01AI122275"],"award-info":[{"award-number":["R01AI132140,R21AI152394,U01AI122275"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"crossref"}]},{"name":"National Cancer Institute","award":["75N91019D00024"],"award-info":[{"award-number":["75N91019D00024"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,11,22]]},"abstract":"<jats:p>\n                    Disseminated coccidioidomycosis (DCM) is caused by\n                    <jats:italic>Coccidioides<\/jats:italic>\n                    , pathogenic fungi endemic to the southwestern United States and Mexico. Illness occurs in approximately 30% of those infected, less than 1% of whom develop disseminated disease. To address why some individuals allow dissemination, we enrolled patients with DCM and performed whole-exome sequencing. In an exploratory set of 67 patients with DCM, 2 had haploinsufficient\n                    <jats:italic>STAT3<\/jats:italic>\n                    mutations, and defects in \u03b2-glucan sensing and response were seen in 34 of 67 cases. Damaging\n                    <jats:italic>CLEC7A<\/jats:italic>\n                    and\n                    <jats:italic>PLCG2<\/jats:italic>\n                    variants were associated with impaired production of \u03b2-glucan\u2013stimulated TNF-\u03b1 from PBMCs compared with healthy controls. Using ancestry-matched controls, damaging\n                    <jats:italic>CLEC7A<\/jats:italic>\n                    and\n                    <jats:italic>PLCG2<\/jats:italic>\n                    variants were overrepresented in DCM, including\n                    <jats:italic>CLEC7A<\/jats:italic>\n                    Y238* and\n                    <jats:italic>PLCG2<\/jats:italic>\n                    R268W. A validation cohort of 111 patients with DCM confirmed the\n                    <jats:italic>PLCG2<\/jats:italic>\n                    R268W,\n                    <jats:italic>CLEC7A<\/jats:italic>\n                    I223S, and\n                    <jats:italic>CLEC7A<\/jats:italic>\n                    Y238* variants. Stimulation with a DECTIN-1 agonist induced DUOX1\/DUOXA1\u2013derived hydrogen peroxide [H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    ] in transfected cells. Heterozygous\n                    <jats:italic>DUOX1<\/jats:italic>\n                    or\n                    <jats:italic>DUOXA1<\/jats:italic>\n                    variants that impaired H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    production were overrepresented in discovery and validation cohorts. Patients with DCM have impaired \u03b2-glucan sensing or response affecting TNF-\u03b1 and H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    production. Impaired\n                    <jats:italic>Coccidioides<\/jats:italic>\n                    recognition and decreased cellular response are associated with disseminated coccidioidomycosis.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.159491","type":"journal-article","created":{"date-parts":[[2022,9,27]],"date-time":"2022-09-27T12:00:46Z","timestamp":1664280046000},"source":"Crossref","is-referenced-by-count":65,"title":["Immunogenetics associated with severe coccidioidomycosis"],"prefix":"10.1172","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6841-2122","authenticated-orcid":true,"given":"Amy P.","family":"Hsu","sequence":"first","affiliation":[{"name":"Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, Maryland, USA."},{"name":"Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, Maryland, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agnieszka","family":"Korzeniowska","sequence":"additional","affiliation":[{"name":"Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, Maryland, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cynthia C.","family":"Aguilar","sequence":"additional","affiliation":[{"name":"Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, Maryland, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2258-3131","authenticated-orcid":true,"given":"Jingwen","family":"Gu","sequence":"additional","affiliation":[{"name":"Bioinformatics and Computational Biosciences Branch, Office of Cyber Infrastructure and Computational Biology, NIAID, NIH, Bethesda, Maryland, 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