ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Delinking CARD9 and IL-17: CARD9 Protects against Candida tropicalis Infection through a TNF-α-Dependent, IL-17-Independent Mechanism.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed, 50 citations in OpenAlex.
- IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Article
- Molecular mechanisms of neutrophil regulatory network in anti-Candida infection.Frontiers in immunology · 2025Review
- Mitochondria-mediated ferroptosis induced by CARD9 ablation prevents MDSCs-dependent antifungal immunity.Cell communication and signaling : CCS · 2024Article
- Dectin-1 aggravates neutrophil inflammation through caspase-11/4-mediated macrophage pyroptosis in asthma.Respiratory research · 2024Article
- Role of CARD9 in Cell- and Organ-Specific Immune Responses in Various Infections.International journal of molecular sciences · 2024Review
- Invasive Candidiasis: Update and Current Challenges in the Management of This Mycosis in South America.Antibiotics (Basel, Switzerland) · 2022Review
- Mitogen-activated protein kinase phosphatase-1 controls PD-L1 expression by regulating type I interferon during systemic Escherichia coli infection.The Journal of biological chemistry · 2022Article
- The Role of B-Cells and Antibodies againstVaccines · 2021Review
- Article
- Role of Protein Mannosylation in theFrontiers in microbiology · 2019Article
- IL-17 in Renal Immunity and Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2018Review
- The evidence for fungus in Crohn's disease pathogenesis.Clinical journal of gastroenterology · 2018Review
- Inherited CARD9 Deficiency: Invasive Disease Caused by Ascomycete Fungi in Previously Healthy Children and Adults.Journal of clinical immunology · 2018Review
- The essential function of CARD9 in diet-induced inflammation and metabolic disorders in mice.Journal of cellular and molecular medicine · 2018Article
- Unexpected kidney-restricted role for IL-17 receptor signaling in defense against systemic Candida albicans infection.JCI insight · 2018Article
- Innate Immunity to Mucosal Candida Infections.Journal of fungi (Basel, Switzerland) · 2017Review
- Fungal dysbiosis: immunity and interactions at mucosal barriers.Nature reviews. Immunology · 2017Review
- The Role of IL-17 in Protection against Mucosal Candida Infections.Journal of fungi (Basel, Switzerland) · 2017Review
- Chronic Candidiasis in Children.Current allergy and asthma reports · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Candida is the third most common cause of bloodstream infections in hospitalized patients. Immunity to C. albicans, the most frequent species to be isolated in candidiasis, involves a well-characterized Dectin-1/caspase-associated recruitment domain adaptor 9 (CARD9)/IL-17 signaling axis. Infections caused by non-albicans Candida species are on the rise, but surprisingly little is known about immunity to these pathogens. In this study, we evaluated a systemic infection model of C. tropicalis, a clinically relevant, but poorly understood, non-albicans Candida. Mice lacking CARD9 were profoundly susceptible to C. tropicalis, displaying elevated fungal burdens in visceral organs and increased mortality compared with wild-type (WT) controls. Unlike C. albicans, IL-17 responses were induced normally in CARD9(-/-) mice following C. tropicalis infection. Moreover, there was no difference in susceptibility to C. tropicalis infection between WT and IL-23p19(-/-), IL-17RA(-/-), or Act1(-/-) mice. However, TNF-α expression was markedly impaired in CARD9(-/-) mice. Consistently, WT mice depleted of TNF-α were more susceptible to C. tropicalis, and CARD9-deficient neutrophils and monocytes failed to produce TNF-α following stimulation with C. tropicalis Ags. Both neutrophils and monocytes were necessary for defense against C. tropicalis, because their depletion in WT mice enhanced susceptibility to C. tropicalis. Disease in CARD9(-/-) mice was not due to defective neutrophil or monocyte recruitment to infected kidneys. However, TNF-α treatment of neutrophils in vitro enhanced their ability to kill C. tropicalis. Thus, protection against systemic C. tropicalis infection requires CARD9 and TNF-α, but not IL-17, signaling. Moreover, CARD9-dependent production of TNF-α enhances the candidacidal capacity of neutrophils, limiting fungal disease during disseminated C. tropicalis infection.
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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.