ArticlePLoS pathogens2019
Candida albicans triggers NADPH oxidase-independent neutrophil extracellular traps through dectin-2.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 82 citations in OpenAlex.
- Study on the pro-inflammatory injury of neutrophil extracellular traps in gouty nephropathy.Frontiers in immunology · 2026Review
- Commentary: Tumor associated neutrophils promote prostate cancer progression by mediating neutrophil trap secretion through PSMA1- NF-κB-HIF-1α signaling axis.Frontiers in immunology · 2026Article
- Neutrophil extracellular traps in antifungal immunity: mechanisms, dual roles, regulatory networks, and clinical perspectives.Frontiers in cellular and infection microbiology · 2026Review
- Sex-dependent effects of peptidylarginine deiminases on neutrophil function and long-term outcomes after spinal cord injury.Experimental neurology · 2025Article
- FHL2 deficiency aggravates Candida albicans infection through decreased myelopoiesis.Science China. Life sciences · 2025Article
- Molecular mechanisms of neutrophil regulatory network in anti-Candida infection.Frontiers in immunology · 2025Review
- Antifungal Innate Immunity.Advances in experimental medicine and biology · 2025Review
- Neutrophil and neutrophil extracellular traps in acute kidney injury: from mechanisms to treatments.Frontiers in immunology · 2025Review
- Multi-omics analysis reveals neutrophil heterogeneity and key molecular drivers in sepsis-associated acute kidney injury.Frontiers in immunology · 2025Article
- The Dectin-1 and Dectin-2 clusters: C-type lectin receptors with fundamental roles in immunity.EMBO reports · 2024Review
- The Role of Vitamin D3 Deficiency and Colonization of the Oral Mucosa byJournal of clinical medicine · 2024Review
- Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris.PLoS pathogens · 2024Article
- Review
- Impaired neutrophil extracellular trap-forming capacity contributes to susceptibility to chronic vaginitis in a mouse model of vulvovaginal candidiasis.Infection and immunity · 2024Article
- Candida albicans induces neutrophil extracellular traps and leucotoxic hypercitrullination via candidalysin.EMBO reports · 2023Article
- How metals fuel fungal virulence, yet promote anti-fungal immunity.Disease models & mechanisms · 2023Review
- The Interplay betweenMicroorganisms · 2023Review
- Synovial fluid neutrophil extracellular traps could improve the diagnosis of periprosthetic joint infection.Bone & joint research · 2023Article
- C-type lectin receptor expression is a hallmark of neutrophils infiltrating the skin in epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- High expression of P-selectin induces neutrophil extracellular traps via the PSGL-1/Syk/CaFrontiers in immunology · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Candida albicans is one of the top leading causes of healthcare-associated bloodstream infection. Neutrophil extracellular traps (NET) are known to capture and kill pathogens. It is reported that opsonized C. albicans-triggered NETosis is NADPH oxidase-dependent. We discovered a NADPH oxidase-independent NETosis pathway in neutrophil response to unopsonized C. albicans. While CR3 engagement with opsonized C. albicans triggered NET, dectin-2 recognized unopsonized C. albicans and mediated NET formation. Engagement of dectin-2 activated the downstream Syk-Ca2+-PKCδ-protein arginine deiminase 4 (PAD4) signaling pathway which modulated nuclear translocation of neutrophil elastase (NE), histone citrullination and NETosis. In a C. albicans peritonitis model we observed Ki67+Ly6G+ NETotic cells in the peritoneal exudate and mesenteric tissues within 3 h of infection. Treatment with PAD4 inhibitor GSK484 or dectin-2 deficiency reduced % Ki67+Ly6G+ cells and the intensity of Ki67 in peritoneal neutrophils. Employing DNA digestion enzyme micrococcal nuclease, GSK484 as well as dectin-2-deficient mice, we further showed that dectin-2-mediated PAD4-dependent NET formation in vivo restrained the spread of C. albicans from the peritoneal cavity to kidney. Taken together, this study reveals that unopsonized C. albicans evokes NADPH oxidase-independent NETosis through dectin-2 and its downstream signaling pathway and dectin-2-mediated NET helps restrain fungal dissemination.
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