ArticleInfection and immunity2008
The opportunistic human pathogenic fungus Aspergillus fumigatus evades the host complement system.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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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Who cites it
52 citing papers in PubMed, 115 citations in OpenAlex.
- Spatial proteomics for the analysis of host-pathogen interactions in mice lungs infected withmicroLife · 2026Article
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Antifungal Innate Immunity.Advances in experimental medicine and biology · 2025Review
- Immunity to fungi and vaccine considerations.Cell host & microbe · 2024Review
- Fungal resilience and host-pathogen interactions: Future perspectives and opportunities.Parasite immunology · 2023Review
- Microbial evasion of the complement system: a continuous and evolving story.Frontiers in immunology · 2023Review
- Protective role of host complement system inFrontiers in immunology · 2022Article
- Review
- Fungal Melanin and the Mammalian Immune System.Journal of fungi (Basel, Switzerland) · 2021Review
- Discovery of fungal surface NADases predominantly present in pathogenic species.Nature communications · 2021Article
- Brain death-induced lung injury is complement dependent, with a primary role for the classical/lectin pathway.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021Article
- Proteomic Analysis of Humoral Immune Components in Bronchoalveolar Lavage of Patients Infected or Colonized byFrontiers in immunology · 2021Article
- Article
- A transcriptional signature accurately identifies Aspergillus Infection across healthy and immunosuppressed states.Translational research : the journal of laboratory and clinical medicine · 2020Article
- Review
- Hybrid Agent-Based Modeling ofFrontiers in microbiology · 2020Article
- Local Activation of the Alternative Pathway of Complement System in Mycotic Keratitis Patient Tear.Frontiers in cellular and infection microbiology · 2020Article
- Antivirulence and avirulence genes in human pathogenic fungi.Virulence · 2019Review
- Solubilized melanin suppresses macrophage function.FEBS open bio · 2019Article
- Enolase FromFrontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The opportunistic human pathogenic fungus Aspergillus fumigatus causes severe systemic infections and is a major cause of fungal infections in immunocompromised patients. A. fumigatus conidia activate the alternative pathway of the complement system. In order to assess the mechanisms by which A. fumigatus evades the activated complement system, we analyzed the binding of host complement regulators to A. fumigatus. The binding of factor H and factor H-like protein 1 (FHL-1) from human sera to A. fumigatus conidia was shown by adsorption assays and immunostaining. In addition, factor H-related protein 1 (FHR-1) bound to conidia. Adsorption assays with recombinant factor H mutants were used to localize the binding domains. One binding region was identified within N-terminal short consensus repeats (SCRs) 1 to 7 and a second one within C-terminal SCR 20. Plasminogen was identified as the fourth host regulatory molecule that binds to A. fumigatus conidia. In contrast to conidia, other developmental stages of A. fumigatus, like swollen conidia or hyphae, did not bind to factor H, FHR-1, FHL-1, and plasminogen, thus indicating the developmentally regulated expression of A. fumigatus surface ligands. Both factor H and plasminogen maintained regulating activity when they were bound to the conidial surface. Bound factor H acted as a cofactor to the factor I-mediated cleavage of C3b. Plasminogen showed proteolytic activity when activated to plasmin by urokinase-type plasminogen activator. These data show that A. fumigatus conidia bind to complement regulators, and these bound host regulators may contribute to evasion of a host complement attack.
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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.