ArticlePLoS pathogens2025
The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Pathogenicity and virulence ofVirulence · 2026Review
- Candida auris uses nutrient sensing to modulate virulence and host immune responses.Nature microbiology · 2026Article
- Article
- Article
- Diabetes and Immunosuppression Drive Distinct Patterns ofbioRxiv : the preprint server for biology · 2026Article
- β-Glucan chitosan particle provides cross-protection against multi-drug-resistant Candida auris.NPJ vaccines · 2026Article
- Review
- Host-Candida auris interactions in the skin.PLoS pathogens · 2026Review
- Tackling a global threat: a clinical scenario-based framework for preventing and managingFrontiers in cellular and infection microbiology · 2026Review
- Review
- Emergence, function, and therapeutic strategies to target the PD-1/PD-L1 immune checkpoint during pathogenic fungal infections.Virulence · 2025Review
- β-Glucan Chitosan Particle Provides Cross-Protection Against Multi-Drug- Resistant Candida auris.Research square · 2025Article
- Article
- Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Candida auris is an emerging multidrug-resistant skin-tropic fungal pathogen that causes serious human infections. However, the factors that regulate C. auris skin infection in vivo are still unclear. In this study, we identified that, unlike Candida albicans, which induces IL-17-secreting protective effector Th17 cells, C. auris predominately induces IFNγ-secreting pathogenic Th1 cells during reinfection. Surprisingly, we found that IFNγ enhances skin infection of C. auris but not C. albicans. Mechanistically, IFNγ enhances skin infection of C. auris by dampening the protective IL-17 responses and increasing dermal damage. Furthermore, we identified that the development of Th1 cells occurs through IL-12, produced by C. auris-induced inflammatory macrophages and monocyte-derived dendritic cells. In addition, our findings reveal that C. auris unique cell wall outer mannan layer regulates the development of Th1 and Th17 cells. Collectively, our findings, for the first time, identified that C. auris induces IFNγ to persist in the skin. These findings help explain why C. auris but not C. albicans preferentially persist in the skin long-term, with the potential to identify novel therapeutic approaches to prevent and treat this emerging fungal pathogen in humans.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.