{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T13:52:19Z","timestamp":1791381139844,"version":"4.3.3"},"reference-count":25,"publisher":"American Society for Microbiology","license":[{"start":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:00Z","timestamp":1791331200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100017540","name":"Division of Intramural Research","doi-asserted-by":"publisher","award":["ZIA AI001175"],"award-info":[{"award-number":["ZIA AI001175"]}],"id":[{"id":"10.13039\/100017540","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>Oral candidiasis arises from either genetic immune defects or iatrogenic immune suppression, most commonly due to corticosteroid therapy. Although the cortisone acetate mouse model is widely used to study corticosteroid-associated oral candidiasis, the underlying mechanisms of susceptibility remain poorly defined. Here, we show that corticosteroid-induced susceptibility to oral candidiasis is driven primarily by impairment of type-17 immunity. In contrast, interferon-gammopathy, another immune state known to promote oral candidiasis, does not contribute to disease in the cortisone model. Moreover, interferon-gammopathy is not required for susceptibility to oral candidiasis in the setting of type-17 signaling deficiency. Taken together, these findings demonstrate that type-17 immune deficiency and interferon-gammopathy represent independent, non-overlapping pathways to oral candidiasis and establish impaired type-17 immunity as the dominant mechanism underlying corticosteroid-induced disease.<\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Candida albicans<\/jats:italic>\n                        normally lives harmlessly in the mouth, but overgrowth can cause oral candidiasis, a painful infection that can interfere with eating and swallowing. One of the most common causes of oral candidiasis is treatment with corticosteroids, medications that are widely used to control autoimmune and allergic diseases. Although corticosteroids are known to weaken immune defenses, it is unknown which immune pathways are impaired to promote susceptibility to this infection. We show that corticosteroids promote oral candidiasis by suppressing a specific protective immune response, known as type-17 immunity, rather than by triggering excessive inflammatory responses driven by interferon-\u03b3. We further demonstrate that these two immune alterations\u2014loss of type-17 immunity and interferon-\u03b3-driven inflammation\u2014cause oral candidiasis through independent mechanisms. These findings clarify how corticosteroids predispose patients to oral candidiasis and refine our understanding of the immune pathways that normally protect the oral mucosa.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.02170-26","type":"journal-article","created":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T13:00:59Z","timestamp":1791378059000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Corticosteroids drive oral candidiasis by impairing type-17 immunity without inducing interferon-gammopathy"],"prefix":"10.1128","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0271-0562","authenticated-orcid":true,"given":"Ashira","family":"Lubkin","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/045p44t13","id-type":"ROR","asserted-by":"publisher"}],"name":"Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institutes of Health, National Institute of Allergy and Infectious Diseases","place":["Bethesda, USA"]},{"id":[{"id":"https:\/\/ror.org\/045p44t13","id-type":"ROR","asserted-by":"publisher"}],"name":"Postdoctoral Research Associate Program, National Institute of General Medical Sciences, National Institutes of Health","place":["Bethesda, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abigail","family":"Fellows","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/045p44t13","id-type":"ROR","asserted-by":"publisher"}],"name":"Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institutes of Health, National Institute of Allergy and Infectious Diseases","place":["Bethesda, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucas","family":"dos Santos Dias","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/045p44t13","id-type":"ROR","asserted-by":"publisher"}],"name":"Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institutes of Health, National Institute of Allergy and Infectious Diseases","place":["Bethesda, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vasileios","family":"Oikonomou","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/045p44t13","id-type":"ROR","asserted-by":"publisher"}],"name":"Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institutes of Health, National Institute of Allergy and Infectious Diseases","place":["Bethesda, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4994-9500","authenticated-orcid":true,"given":"Michail S.","family":"Lionakis","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/045p44t13","id-type":"ROR","asserted-by":"publisher"}],"name":"Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institutes of Health, National Institute of Allergy and Infectious Diseases","place":["Bethesda, 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