ArticleThe Journal of infectious diseases2007
Immune recognition of Candida albicans beta-glucan by dectin-1.
Article in The Journal of infectious diseases, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers.
What it found
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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.
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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
189 citing papers in PubMed, 312 citations in OpenAlex.
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- Candida albicans infection suppresses lipopolysaccharide or Pseudomonas aeruginosa stimulated murine bone marrow derived macrophage (BMDM) responses.Scientific reports · 2026Article
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- Synthetic Lethal Therapy Based on Dimorphism for Systemic Infection of Drug-Resistant Candida albicans.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- Molecular mechanisms, pathogenesis and therapeutic advances ofFrontiers in cellular and infection microbiology · 2026Review
- Candida albicans Cells Lacking AP-2 Have Defective Hyphae and Are Avirulent Despite Increased Host Uptake and Intracellular Proliferation in Macrophages.Molecular microbiology · 2026Article
- The trio of Candida albicans, immune cells, and cancer progression: a complex interplay driving tumorigenesis.Medical oncology (Northwood, London, England) · 2025Review
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- Dectin-1 and dectin-2 drive protection againstFrontiers in immunology · 2025Article
- Exploring the structural basis and functional immunodynamics of immunoglobulin M in host defense against fungal pathogens.Frontiers in immunology · 2025Review
- Candida albicans N-Linked Mannans Potentiate the Induction of Trained Immunity via Dectin-2.The Journal of infectious diseases · 2024Article
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- Comparative Evaluation ofBiomedicines · 2024Article
- Review
129 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
15 authors at 3 institutions in 3 countries.
Funding
Abstract
Beta (1,3)-glucans represent 40% of the cell wall of the yeast Candida albicans. The dectin-1 lectin-like receptor has shown to recognize fungal beta (1,3)-glucans and induce innate immune responses. The importance of beta-glucan-dectin-1 pathways for the recognition of C. albicans by human primary blood cells has not been firmly established. In this study we demonstrate that cytokine production by both human peripheral blood mononuclear cells and murine macrophages is dependent on the recognition of beta-glucans by dectin-1. Heat killing of C. albicans resulted in exposure of beta-glucans on the surface of the cell wall and subsequent recognition by dectin-1, whereas live yeasts stimulated monocytes mainly via recognition of cell-surface mannans. Dectin-1 induced cytokine production through the following 2 pathways: Syk-dependent production of the T-helper (Th) 2-type anti-inflammatory cytokine interleukin-10 and Toll-like receptor-Myd88-dependent stimulation of monocyte-derived proinflammatory cytokines, such as tumor necrosis factor-alpha . In contrast, stimulation of Th1-type cytokines, such as interferon-gamma , by C. albicans was independent of the recognition of beta-glucans by dectin-1. In conclusion, C. albicans induces production of monocyte-derived and T cell-derived cytokines through distinct pathways dependent on or independent of dectin-1.
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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.