ArticleScientific reports2025
Candida albicans aspartyl protease (Sap6) inhibits neutrophil function via a "Trojan horse" mechanism.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Genome-Wide Identification and Expression Analysis of the Aspartic Protease Gene Family and Their Responses to Abiotic Stress inMicroorganisms · 2026Article
- Innate airway immune response to fungal allergens.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps in antifungal immunity: mechanisms, dual roles, regulatory networks, and clinical perspectives.Frontiers in cellular and infection microbiology · 2026Review
- Review
- Wss1 and Ddi1 DNA-Protein crosslink repair proteases protect Saccharomyces cerevisiae and Candida albicans against oxidative stress.Scientific reports · 2025Article
- Extracellular vesicles from bacteria and fungi: mechanistic insights and implications for urinary tract infections.Extracellular vesicles and circulating nucleic acids · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Candida albicans, a prevalent fungal pathogen, employs aspartyl proteases such as Sap6 to evade immune defenses, challenging our understanding of host‒pathogen interactions. This research examined the impact of Sap6 on neutrophil responses, which are crucial for innate immunity. Employing flow cytometry and fluorescence microscopy, we explored how Sap6 affects neutrophil functions, particularly by focusing on reactive oxygen species (ROS) production, neutrophil extracellular traps release (NETosis), and apoptosis. Our findings revealed Sap6's unique ability to bind and internalize in neutrophils, significantly attenuating ROS production through proteolytic damage to NADPH oxidase, resulting in blocking the ROS-dependent NETosis pathway. This disruption in neutrophil functions by Sap6 suggested the presence of a 'Trojan horse' mechanism by C. albicans. This mechanism reveals a sophisticated immune evasion strategy, shedding light on fungal pathogenicity and host immune interactions. Understanding fungal proteases in immune modulation could inspire new therapeutic approaches for fungal infections.
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Registered trials
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