ArticleNature communications2016
Neutrophil-specific deletion of the CARD9 gene expression regulator suppresses autoantibody-induced inflammation in vivo.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 72 citations in OpenAlex.
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- Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis.Nature communications · 2026Article
- Tyrosine kinase signaling pathways as therapeutic targets in autoimmune subepidermal blistering skin diseases (pemphigoid diseases).Frontiers in immunology · 2026Review
- Calprotectin as a Biomarker for Infectious Diseases: A Comparative Review with Conventional Inflammatory Markers.International journal of molecular sciences · 2025Review
- ARHGAP25: a novel player in the Pathomechanism of allergic contact hypersensitivity.Frontiers in immunology · 2025Article
- Pemphigoid disease model systems for clinical translation.Frontiers in immunology · 2025Review
- Neutrophils Expressing Programmed Death-Ligand 1 Play an Indispensable Role in Effective Bacterial Elimination and Resolving Inflammation in Methicillin-ResistantPathogens (Basel, Switzerland) · 2024Article
- Increased susceptibility to Mycobacterium avium complex infection in miniature Schnauzer dogs caused by a codon deletion in CARD9.Scientific reports · 2024Article
- CARD9 in the pathogenesis of axial spondyloarthritis.Best practice & research. Clinical rheumatology · 2024Review
- Card9/neutrophil signalling axis promotes IL-17A-mediated ankylosing spondylitis.Annals of the rheumatic diseases · 2024Article
- Disruption of hypoxia-inducible factor-2α in neutrophils decreases colitis-associated colon cancer.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Inhibition of interferon gamma impairs induction of experimental epidermolysis bullosa acquisita.Frontiers in immunology · 2024Article
- Macrophage CARD9 mediates cardiac injury following myocardial infarction through regulation of lipocalin 2 expression.Signal transduction and targeted therapy · 2023Article
- Myeloid Src-family kinases are critical for neutrophil-mediated autoinflammation in gout and motheaten models.The Journal of experimental medicine · 2023Article
- The selective inhibition of the Syk tyrosine kinase ameliorates experimental autoimmune arthritis.Frontiers in immunology · 2023Article
- PD-L1 negatively regulates antifungal immunity by inhibiting neutrophil release from bone marrow.Nature communications · 2022Article
- Dysregulated lipolysis and lipophagy in lipid droplets of macrophages from high fat diet-fed obese mice.Journal of cellular and molecular medicine · 2022Article
- Cutaneous kinase activity correlates with treatment outcomes following PI3K delta inhibition in mice with experimental pemphigoid diseases.Frontiers in immunology · 2022Article
- CARD9 Signaling, Inflammation, and Diseases.Frontiers in immunology · 2022Review
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5 authors at 4 institutions in 2 countries.
Funding
Abstract
Neutrophils are terminally differentiated cells with limited transcriptional activity. The biological function of their gene expression changes is poorly understood. CARD9 regulates transcription during antifungal immunity but its role in sterile inflammation is unclear. Here we show that neutrophil CARD9 mediates pro-inflammatory chemokine/cytokine but not lipid mediator release during non-infectious inflammation. Genetic deficiency of CARD9 suppresses autoantibody-induced arthritis and dermatitis in mice. Neutrophil-specific deletion of CARD9 is sufficient to induce that phenotype. Card9(-/-) neutrophils show defective immune complex-induced gene expression changes and pro-inflammatory chemokine/cytokine release but normal LTB4 production and other short-term responses. In vivo deletion of CARD9 reduces tissue levels of pro-inflammatory chemokines and cytokines but not LTB4. The CARD9-mediated signalling pathway involves Src-family kinases, Syk, PLCγ2, Bcl10/Malt1 and NFκB. Collectively, CARD9-mediated gene expression changes within neutrophils play important roles during non-infectious inflammation in vivo and CARD9 acts as a divergence point between chemokine/cytokine and lipid mediator release.
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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.