ArticlePLoS pathogens2019
The protective effect of inflammatory monocytes during systemic C. albicans infection is dependent on collaboration between C-type lectin-like receptors.
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 35 papers.
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Who cites it
35 citing papers in PubMed, 50 citations in OpenAlex.
- IL-1 family signalling drives mucosal defence against systemic Candida albicans infection.Nature microbiology · 2026Article
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- Vacuolar sterol β-glucosidase EGCrP2/Sgl1 deficiency in Cryptococcus neoformans: Dysfunctional autophagy and Mincle-dependent immune activation as targets of novel antifungal strategies.PLoS pathogens · 2025Article
- Unveiling the fungal frontier: mycological insights into inflammatory bowel disease.Frontiers in immunology · 2025Review
- BLNK negatively regulates innate antifungal immunity through inhibiting c-Cbl-mediated macrophage migration.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Adhesin Antibody-Grafted Mesoporous Silica Nanoparticles Suppress Immune Escape for Treatment of Fungal Systemic Infection.Molecules (Basel, Switzerland) · 2024Article
- Macrophage fate: to kill or not to kill?Infection and immunity · 2024Review
- Card9 and MyD88 differentially regulate Th17 immunity to the commensal yeastbioRxiv : the preprint server for biology · 2024Article
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- Cell-intrinsic C5a synergizes with Dectin-1 in macrophages to mediate fungal killing.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Phagosomal signalling of the C-type lectin receptor Dectin-1 is terminated by intramembrane proteolysis.Nature communications · 2022Article
- LncRNA: A Potential Target for Host-Directed Therapy ofPharmaceutics · 2022Review
- When Is It Appropriate to Take Off the Mask? Signaling Pathways That Regulate ß(1,3)-Glucan Exposure inFrontiers in fungal biology · 2022Article
- Review
- Control of β-glucan exposure by the endo-1,3-glucanase Eng1 in Candida albicans modulates virulence.PLoS pathogens · 2022Article
- Evaluation of Cell Models to Study Monocyte Functions in PMM2 Congenital Disorders of Glycosylation.Frontiers in immunology · 2022Article
- Immunoprofiling of monocytes in STAT1 gain-of-function chronic mucocutaneous candidiasis.Frontiers in immunology · 2022Article
- Carbohydrates from Pseudomonas aeruginosa biofilms interact with immune C-type lectins and interfere with their receptor function.NPJ biofilms and microbiomes · 2021Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Invasive candidiasis, mainly caused by Candida albicans, is a serious healthcare problem with high mortality rates, particularly in immunocompromised patients. Innate immune cells express pathogen recognition receptors (PRRs) including C-type lectin-like receptors (CLRs) that bind C. albicans to initiate an immune response. Multiple CLRs including Dectin-1, Dectin-2 and Mincle have been proposed individually to contribute to the immune response to C. albicans. However how these receptors collaborate to clear a fungal infection is unknown. Herein, we used novel multi-CLR knockout (KO) mice to decipher the individual, collaborative and collective roles of Dectin-1, Dectin-2 and Mincle during systemic C. albicans infection. These studies revealed an unappreciated and profound role for CLR co-operation in anti-fungal immunity. The protective effect of multiple CLRs was markedly greater than any single receptor, and was mediated through inflammatory monocytes via recognition and phagocytosis of C. albicans, and production of C. albicans-induced cytokines and chemokines. These CLRs were dispensable for mediating similar responses from neutrophils, likely due to lower expression of these CLRs on neutrophils compared to inflammatory monocytes. Concurrent deletion of Dectin-1 and Dectin-2, or all three CLRs, resulted in dramatically increased susceptibility to systemic C. albicans infection compared to mice lacking a single CLR. Multi-CLR KO mice were unable to control fungal growth due to an inadequate early inflammatory monocyte-mediated response. In response to excessive fungal growth, the multi-CLR KO mice mounted a hyper-inflammatory response, likely leading to multiple organ failure. Thus, these data reveal a critical role for CLR co-operation in the effective control of C. albicans and maintenance of organ function during infection.
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