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Cited by 175Immunodeficiency and Autoimmune DisordersAntifungal resistance and susceptibilityT-cell and B-cell Immunology

Aberrant type 1 immunity drives susceptibility to mucosal fungal infections.

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Break, Timothy J., Oikonomou, Vasileios, Dutzan, Nicolas, Desai, Jigar V., Swidergall, Marc, Freiwald, Tilo, Chauss, Daniel, Harrison, Oliver J. +35 more·2021·Science
DOI 10.1126/science.aay5731PMC PMC8326743
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Abstract

Type 1 immunity gives fungi a foothold: 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 Candida albicans prominently infects patients with autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy (APECED), an inherited disease caused by loss-of-function mutations in the AIRE gene. Break et al. report that the oral susceptibility of Aire -deficient mice to C. albicans is not due to aberrant type 17 responses. Rather, the overproduction of interferon-γ by local CD4 + and CD8 + T cells in these mice disrupts the epithelial barrier, which increases susceptibility to C. albicans invasion. Similar type 1 immune pathways are operational in APECED patients. Inhibition of interferon-γ or the JAK-STAT signaling pathway in mice ameliorates disease symptoms, suggesting potential future therapeutic interventions for certain classes of fungal disease. Science , this issue p. eaay5731

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  • IFN-γ induces apoptosis in epithelial cells and fibroblasts and can enhance cell-mediated cytotoxicity.

    “Since IFN-γ induces apoptosis in epithelial cells and fibroblasts and can enhance cell-mediated cytotoxicity [21–23], we examined if the increased production of IFN-γ in C. auris-infected mice might promote increased cell death and enhance fungal burden.”

    From The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin (2025) · cites this paper as [21]

    The section on IFN-γ/STAT1 responses in AIRE deficiency (page not provided) reports dose-dependent death of human oral epithelial cells after prolonged IFN-γ exposure. It does not establish that the death was apoptosis, and the cited passages do not support the claims about fibroblasts or enhanced cell-mediated cytotoxicity. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • IFN-γ drives apoptosis of epithelial cells and fibroblasts and disrupts barrier integrity.

    “Secondly, IFN-γ drives apoptosis of epithelial cells and fibroblasts and disrupts barrier integrity [117–119].”

    From Host–Candida auris interactions in the skin (2026) · cites this paper as [117]

    In the section on IFN-γ/STAT1 responses in AIRE deficiency (page not provided), prolonged IFN-γ exposure caused death of human oral epithelial cells and increased epithelial permeability, supporting the barrier-integrity part of the claim. The paper does not identify that cell death as apoptosis or report IFN-γ-induced fibroblast death. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Excess IFN-γ responses can impair the oral mucosal barrier and drive oral C. albicans infection during AIRE deficiency.

    “Previous findings from the Lionakis lab suggest that excess IFN-γ responses can impair the oral mucosal barrier and drive oral C. albicans infection during AIRE deficiency [21].”

    From The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin (2025) · cites this paper as [21]

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Authors
Break, T. J., Oikonomou, V., Dutzan, N., Desai, J. V., Swidergall, M., Freiwald, T., Chauss, D., Harrison, O. J., Alejo, J., Williams, D. W., Pittaluga, S., Lee, C.-C. R., Bouladoux, N., Swamydas, M., Hoffman, K. W., Greenwell-Wild, T., Bruno, V. M., Rosen, L. B., Lwin, W., Renteria, A., Pontejo, S. M., Shannon, J. P., Myles, I. A., Olbrich, P., Ferré, E. M. N., Schmitt, M., Martin, D., Core, G. A. C. B., Barber, D. L., Solis, N. V., Notarangelo, L. D., Serreze, D. V., Matsumoto, M., Hickman, H. D., Murphy, P. M., Anderson, M. S., Lim, J. K., Holland, S. M., Filler, S. G., Afzali, B., Belkaid, Y., Moutsopoulos, N. M., & Lionakis, M. S.
Affiliations
  • National Institute of Allergy and Infectious Diseases (US)
  • Oral Immunity and Inflammation Section, National Institute of Dental and Craniofacial Research (NIDCR), Bethesda, MD, USA.
  • University of California, Los Angeles (US)
  • National Institute of Diabetes and Digestive and Kidney Diseases (US)
  • National Cancer Institute (US)
  • National Institute of Dental and Craniofacial Research (US)
  • Icahn School of Medicine at Mount Sinai (US)
  • University of Maryland, Baltimore (US)
  • National Institutes of Health (US)
  • University of California, San Francisco (US)
  • Genomics and Computational Biology Core, NIDCR, Bethesda, MD, USA.
  • The Lundquist Institute (US)
  • Jackson Laboratory (US)
Corresponding author
  • Break, Timothy J.
  • Oikonomou, Vasileios
  • Lionakis, Michail S.
ORCID
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
2021-01-15
Volume
371
Issue
6526
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
DOI
10.1126/science.aay5731
PMC
PMC8326743
OpenAlex
W3120375284
Cited by
175
References
9
Citations by year
2026: 29 · 2025: 24 · 2024: 39 · 2023: 27 · 2022: 34 · 2021: 22
FWCI
11.38
Type
journal article
Language
en
Open access
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
  • The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
Funders
Division of Intramural Research, National Institute of Allergy and Infectious Diseases
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
type 1 immune response, Candida albicans, APECED, AIRE deficiency, interferon-gamma, CD4+ T cells, CD8+ T cells, epithelial barrier function, JAK/STAT signaling, oral candidiasis, host defense against fungi
MeSH terms
Interleukin-22, Adolescent, Adult, Aged, Animals, Candida albicans, Candidiasis, Chronic Mucocutaneous, Disease Models, Animal, Female, Humans, Immunologic Surveillance, Interferon-gamma, Interleukins, Male, Mice, Inbred BALB C, Middle Aged, Mouth Mucosa, T-Lymphocytes, Polyendocrinopathies, Autoimmune, Immunity, Mucosal, STAT1 Transcription Factor, Mice, Janus Kinases, Receptors, Interleukin-17, Young Adult

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