ArticlePLoS pathogens2012
Type I interferons promote fatal immunopathology by regulating inflammatory monocytes and neutrophils during Candida infections.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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Who cites it
106 citing papers in PubMed, 160 citations in OpenAlex.
- CLEC-1 promotes early IFN response in cDC1s and favors immune dysregulation during sepsis in mice.iScience · 2026Article
- Type I interferon signaling promotes mucosal inflammation in murine models of colitis.bioRxiv : the preprint server for biology · 2026Article
- Glycolysis-dependent sulfur metabolism orchestrates morphological plasticity and virulence in fungi.eLife · 2026Article
- IL-17-mediated antifungal immunity restricts Candida albicans pathogenicity in the oral cavity.Nature microbiology · 2026Article
- Cytosolic receptors and signaling in antifungal immunity.The EMBO journal · 2025Review
- Article
- Anti-Inflammatory Potential of Extracellular Polysaccharide from the Moss EndophyteMicroorganisms · 2025Article
- Human Brain Organoids: A New Model to StudyJournal of fungi (Basel, Switzerland) · 2025Article
- Antifungal Innate Immunity.Advances in experimental medicine and biology · 2025Review
- Lack of TYK2 signaling enhances host resistance to Candida albicans skin infection.Nature communications · 2024Article
- MAP2K1 dampens cigarette smoke-induced inflammation via suppression of type I interferon pathway activation.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Adhesin Antibody-Grafted Mesoporous Silica Nanoparticles Suppress Immune Escape for Treatment of Fungal Systemic Infection.Molecules (Basel, Switzerland) · 2024Article
- AIM2 enhances Candida albicans infection through promoting macrophage apoptosis via AKT signaling.Cellular and molecular life sciences : CMLS · 2024Article
- Involvement of cGAS/STING Signaling in the Pathogenesis of Candida albicans Keratitis: Insights From Genetic and Pharmacological Approaches.Investigative ophthalmology & visual science · 2024Article
- MDA5 Enhances Invasive Candida albicans Infection by Regulating Macrophage Apoptosis and Phagocytosis/Killing Functions.Inflammation · 2024Article
- Candida albicans extracellular vesicles trigger type I IFN signalling via cGAS and STING.Nature microbiology · 2024Article
- TRIM26 alleviates fatal immunopathology by regulating inflammatory neutrophil infiltration during Candida infection.PLoS pathogens · 2024Article
- The FVirulence · 2023Article
- Inflammatory ER stress responses dictate the immunopathogenic progression of systemic candidiasis.The Journal of clinical investigation · 2023Article
- Dectin-1 stimulation promotes a distinct inflammatory signature in the setting of HIV-infection and aging.Aging · 2023Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Invasive fungal infections by Candida albicans (Ca) are a frequent cause of lethal sepsis in intensive care unit patients. While a contribution of type I interferons (IFNs-I) in fungal sepsis remains unknown, these immunostimulatory cytokines mediate the lethal effects of endotoxemia and bacterial sepsis. Using a mouse model lacking a functional IFN-I receptor (Ifnar1⁻/⁻), we demonstrate a remarkable protection against invasive Ca infections. We discover a mechanism whereby IFN-I signaling controls the recruitment of inflammatory myeloid cells, including Ly6C(hi) monocytes and neutrophils, to infected kidneys by driving expression of the chemokines CCL2 and KC. Within kidneys, monocytes differentiate into inflammatory DCs but fail to functionally mature in Ifnar1⁻/⁻ mice, as demonstrated by the impaired upregulation of the key activation markers PDCA1 and iNOS. The increased activity of inflammatory monocytes and neutrophils results in hyper-inflammation and lethal kidney pathology. Pharmacological diminution of monocytes and neutrophils by treating mice with pioglitazone, a synthetic agonist of the nuclear receptor peroxisome proliferator-activated receptor-γ (PPAR-γ), strongly reduces renal immunopathology during Ca infection and improves mouse survival. Taken together, our data connect for the first time the sepsis-promoting functions of IFNs-I to the CCL2-mediated recruitment and the activation of inflammatory monocytes/DCs with high host-destructing potency. Moreover, our data demonstrate a therapeutic relevance of PPAR-γ agonists for microbial infectious diseases where inflammatory myeloid cells may contribute to fatal tissue damage.
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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.