ArticleThe Journal of clinical investigation2019
Dok3-protein phosphatase 1 interaction attenuates Card9 signaling and neutrophil-dependent antifungal immunity.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
23 citing papers in PubMed, 42 citations in OpenAlex.
- Neutrophil extracellular traps in antifungal immunity: mechanisms, dual roles, regulatory networks, and clinical perspectives.Frontiers in cellular and infection microbiology · 2026Review
- Transcriptomic and proteomic profiling of pulmonary mucormycosis reveals a failed activation of host immune response.Frontiers in immunology · 2026Article
- Propofol decreases the resistance of neutrophils to Candida albicans by inhibiting ferroptosis and the cGAS-STING pathway.American journal of translational research · 2026Article
- NIF inhibits the ability of PMNs to produce inflammatory cytokines and reactive oxygen species in response toMicrobiology spectrum · 2025Article
- Pretreatment with alendronate augments lipid A-induced IFN-β production via upregulation of cGAS expression.Pharmacological reports : PR · 2025Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- ANKRD22 promotes resolution of psoriasiform skin inflammation by antagonizing NIK-mediated IL-23 production.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look.Frontiers in immunology · 2024Review
- Disrupting the Dok3-Card9 Interaction with Synthetic Peptides Enhances Antifungal Effector Functions of Human Neutrophils.Pharmaceutics · 2023Article
- Neutrophils in the Pathogenesis of Rheumatic Diseases.Rheumatology and immunology research · 2022Review
- Progranulin aggravates lethal Candida albicans sepsis by regulating inflammatory response and antifungal immunity.PLoS pathogens · 2022Article
- CARD9 in host immunity to fungal, bacterial, viral, and parasitic infections: An update.Frontiers in microbiology · 2022Review
- CARD9 Signaling, Inflammation, and Diseases.Frontiers in immunology · 2022Review
- Dok3 restrains neutrophil production of calprotectin during TLR4 sensing of SARS-CoV-2 spike protein.Frontiers in immunology · 2022Article
- The roles of fungus in CNS autoimmune and neurodegeneration disorders.Frontiers in immunology · 2022Review
- DOK3 maintains intestinal homeostasis by suppressing JAK2/STAT3 signaling and S100a8/9 production in neutrophils.Cell death & disease · 2021Article
- NADPH Oxidase Limits Collaborative Pattern-Recognition Receptor Signaling to Regulate Neutrophil Cytokine Production in Response to Fungal Pathogen-Associated Molecular Patterns.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Article
- The Role of CARD9 Deficiency in Neutrophils.Mediators of inflammation · 2021Review
- USP15 Deubiquitinates CARD9 to Downregulate C-Type Lectin Receptor-Mediated Signaling.ImmunoHorizons · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Invasive fungal infection is a serious health threat with high morbidity and mortality. Current antifungal drugs only demonstrate partial success in improving prognosis. Furthermore, mechanisms regulating host defense against fungal pathogens remain elusive. Here, we report that the downstream of kinase 3 (Dok3) adaptor negatively regulates antifungal immunity in neutrophils. Our data revealed that Dok3 deficiency increased phagocytosis, proinflammatory cytokine production, and netosis in neutrophils, thereby enhancing mutant mouse survival against systemic infection with a lethal dose of the pathogenic fungus Candida albicans. Biochemically, Dok3 recruited protein phosphatase 1 (PP1) to dephosphorylate Card9, an essential player in innate antifungal defense, to dampen downstream NF-κB and JNK activation and immune responses. Thus, Dok3 suppresses Card9 signaling, and disrupting Dok3-Card9 interaction or inhibiting PP1 activity represents therapeutic opportunities to develop drugs to combat candidaemia.
Indexed as
Identifiers
What OpenQuestion holds
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.