ArticleProceedings of the National Academy of Sciences of the United States of America2007
Histoplasma capsulatum alpha-(1,3)-glucan blocks innate immune recognition by the beta-glucan receptor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 232 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
232 citing papers in PubMed, 415 citations in OpenAlex.
- Disruption of MaPigA, a phosphatidylinositol-N-acetylglucosaminyltransferase subunit gene, promotes cuticle penetration and immune evasion through enhancing cell wall α-1,3-glucan in Metarhizium anisopliae.Pest management science · 2026Article
- Fungal Infections Associated with Sphingosine 1-Phosphate Receptor Modulators: Immunological Mechanisms, Clinical Patterns, and Management Considerations.Microorganisms · 2026Review
- Immune evasion by a chytrid fungus includes inhibition of macrophage phagocytosis.Infection and immunity · 2026Article
- α-1,3-Glucan-Driven Remodeling of the Conidial Cell Wall in anJournal of the American Chemical Society · 2026Article
- Discovery of a MarineMarine drugs · 2026Article
- Pathogenic mucorales: Deciphering their cell wall polysaccharidome and immunostimulatory potential.Virulence · 2025Article
- Article
- How Histoplasma Evades the Human Immune System.Acta medica academica · 2025Review
- Advancing antifungal therapy: exploring targeted CFW-PEc-enhanced ethosomal formulations of amphotericin B against cryptococcal pneumonia.Microbiology spectrum · 2025Article
- Neuroinflammation in fungal infections: from pathogen recognition to pathological manifestations.Disease models & mechanisms · 2025Review
- Structural and biochemical basis for activity of Aspergillus nidulans α-1,3-glucanases from glycoside hydrolase family 71.Communications biology · 2025Article
- Extracellular vesicles from DistinctACS infectious diseases · 2025Article
- Proteomic Changes inJournal of proteome research · 2025Article
- Protein kinase A signaling regulates immune evasion by shaving and concealing fungal β-1,3-glucan.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Antifungal Innate Immunity.Advances in experimental medicine and biology · 2025Review
- Shape-Shifting Mechanisms: Integrative Multi-Omics Insights IntoMycobiology · 2025Review
- Linear β-1,2-glucans trigger immune hallmarks and enhance disease resistance in plants.Journal of experimental botany · 2024Article
- Article
- United toward a common goal: Coordination of microbial virulence phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Manipulation of host phagocytosis by fungal pathogens and therapeutic opportunities.Nature microbiology · 2024Review
172 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Successful infection by fungal pathogens depends on subversion of host immune mechanisms that detect conserved cell wall components such as beta-glucans. A less common polysaccharide, alpha-(1,3)-glucan, is a cell wall constituent of most fungal respiratory pathogens and has been correlated with pathogenicity or linked directly to virulence. However, the precise mechanism by which alpha-(1,3)-glucan promotes fungal virulence is unknown. Here, we show that alpha-(1,3)-glucan is present in the outermost layer of the Histoplasma capsulatum yeast cell wall and contributes to pathogenesis by concealing immunostimulatory beta-glucans from detection by host phagocytic cells. Production of proinflammatory TNFalpha by phagocytes was suppressed either by the presence of the alpha-(1,3)-glucan layer on yeast cells or by RNA interference based depletion of the host beta-glucan receptor dectin-1. Thus, we have functionally defined key molecular components influencing the initial host-pathogen interaction in histoplasmosis and have revealed an important mechanism by which H. capsulatum thwarts the host immune system. Furthermore, we propose that the degree of this evasion contributes to the difference in pathogenic potential between dimorphic fungal pathogens and opportunistic fungi.
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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.