ReviewFrontiers in immunology2025
Molecular mechanisms of neutrophil regulatory network in anti-Candida infection.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Rethinking the immune recognition of cell walls in human fungal pathogens: Mechanisms, controversies and translational significance.Virulence · 2026Review
- Evaluation of immunological and gene expression responses induced by Galectin-3 and whole-sonicatedOpen veterinary journal · 2026Article
- The Mechanism of G Protein-Coupled Receptor Regulation of Ferroptosis in Hepatic Ischemia-Reperfusion Injury.International journal of molecular sciences · 2026Review
- Gut microbiota-innate immune crosstalk in the initiation and progression of CRC: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- The V-ATPase VJournal of oral microbiology · 2026Article
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 resides as a commensal within the oral mucosa but becomes pathogenic when epithelial or immune equilibrium collapses. Neutrophils constitute the dominant effector population controlling this transition, integrating pathogen- and host-derived cues into a coordinated antimicrobial program. Fungal β-glucan recognition through Dectin-1 and complement receptor 3 (CR3) activates spleen tyrosine kinase (SYK)-phosphoinositide 3-kinase (PI3K)-extracellular signal-regulated kinase (ERK) pathways and drives microtubule-associated protein 1 light chain 3B-II (LC3B-II) accumulation and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome assembly, thereby coupling phagocytosis with oxidative burst and neutrophil extracellular trap (NET) formation. Caspase recruitment domain-containing protein 9 (CARD9)-dependent interleukin (IL)-17 and tumor necrosis factor-α (TNF-α) circuits sustain chemokine (C-X-C motif) ligand 1/2 (CXCL1/2)-directed neutrophil recruitment and granulocyte colony-stimulating factor (G-CSF)-mediated granulopoiesis, while tissue matrix components determine site-specific antigen handling and NETosis thresholds. Hypha-restricted peptide toxin Candidalysin links epithelial injury to NLRP3 activation and release of IL-1β, IL-6, and G-CSF, establishing an oropharyngeal candidiasis (OPC)-specific neutrophil regulatory loop critical for pathogen clearance but also for mucosal inflammation. Conversely, fungal morphogenesis, biofilm organization, and metabolic rewiring dampen reactive oxygen species (ROS) generation and promote immune tolerance and drug resistance. Clinically, G-/granulocyte-macrophage colony-stimulating factor (GM-CSF) adjuvants and G-CSF-mobilized granulocyte transfusion offer context-dependent benefits yet pose toxicity risks, underscoring the need for precise intervention in neutrophil activation. Advances in single-cell and spatial multi-omics approaches are uncovering the metabolic and functional heterogeneity of neutrophils within mucosal environments, providing mechanistic insight for targeted immunomodulation.
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Registered trials
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