{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T03:12:36Z","timestamp":1792033956724,"version":"4.4.0"},"reference-count":74,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6526","funder":[{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2021,1,15]]},"abstract":"<jats:title>Type 1 immunity gives fungi a foothold<\/jats:title>\n                  <jats:p>\n                    Type 17 immune responses play a vital role against fungal infections of the mucosa. It remains unclear whether other types of immune responses can also contribute to host defense against these pathogens. The yeast\n                    <jats:italic>Candida albicans<\/jats:italic>\n                    prominently infects patients with autoimmune polyendocrinopathy\u2013candidiasis\u2013ectodermal dystrophy (APECED), an inherited disease caused by loss-of-function mutations in the\n                    <jats:italic>AIRE<\/jats:italic>\n                    gene. Break\n                    <jats:italic>et al.<\/jats:italic>\n                    report that the oral susceptibility of\n                    <jats:italic>Aire<\/jats:italic>\n                    -deficient mice to\n                    <jats:italic>C. albicans<\/jats:italic>\n                    is not due to aberrant type 17 responses. Rather, the overproduction of interferon-\u03b3 by local CD4\n                    <jats:sup>+<\/jats:sup>\n                    and CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells in these mice disrupts the epithelial barrier, which increases susceptibility to\n                    <jats:italic>C. albicans<\/jats:italic>\n                    invasion. Similar type 1 immune pathways are operational in APECED patients. Inhibition of interferon-\u03b3 or the JAK-STAT signaling pathway in mice ameliorates disease symptoms, suggesting potential future therapeutic interventions for certain classes of fungal disease.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Science<\/jats:italic>\n                    , this issue p.\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" related-article-type=\"in-this-issue\" xlink:href=\"10.1126\/science.aay5731\">eaay5731<\/jats:related-article>\n                  <\/jats:p>","DOI":"10.1126\/science.aay5731","type":"journal-article","created":{"date-parts":[[2021,1,14]],"date-time":"2021-01-14T15:06:30Z","timestamp":1610636790000},"source":"Crossref","is-referenced-by-count":168,"title":["Aberrant type 1 immunity drives susceptibility to mucosal fungal infections"],"prefix":"10.1126","volume":"371","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5987-7817","authenticated-orcid":true,"given":"Timothy J.","family":"Break","sequence":"first","affiliation":[{"name":"Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7553-0159","authenticated-orcid":true,"given":"Vasileios","family":"Oikonomou","sequence":"additional","affiliation":[{"name":"Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, 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