ArticleJournal of immunology (Baltimore, Md. : 1950)2009
App1: an antiphagocytic protein that binds to complement receptors 3 and 2.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
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
35 citing papers in PubMed, 63 citations in OpenAlex.
- Use of a human immortalized microglia cell line to study recognition, phagocytosis, and intracellular survival ofmSphere · 2026Article
- Elements of dissemination in cryptococcosis.mBio · 2024Review
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- Manipulation of host phagocytosis by fungal pathogens and therapeutic opportunities.Nature microbiology · 2024Review
- Inhibition of Microbicidal Activity of Canine Macrophages DH82 Cell Line by Capsular Polysaccharides fromJournal of fungi (Basel, Switzerland) · 2024Article
- Fungal mechanisms of intracellular survival: what can we learn from bacterial pathogens?Infection and immunity · 2023Review
- Structural biology of complement receptors.Frontiers in immunology · 2023Review
- A dissemination-prone morphotype enhances extrapulmonary organ entry by Cryptococcus neoformans.Cell host & microbe · 2022Article
- Categorizing Sequences of Concern by Function To Better Assess Mechanisms of Microbial Pathogenesis.Infection and immunity · 2022Review
- Macrophage Mediated Immunomodulation DuringFrontiers in cellular and infection microbiology · 2022Review
- Camouflage strategies for therapeutic exosomes evasion from phagocytosis.Journal of advanced research · 2021Review
- The Environmental Effects on Virulence Factors and the Antifungal Susceptibility ofInternational journal of molecular sciences · 2021Review
- Fungal immunity and pathogenesis in mammals versus the invertebrate model organism Galleria mellonella.Pathogens and disease · 2021Review
- Dangerous Liaisons: Interactions ofPathogens (Basel, Switzerland) · 2020Review
- Cell Wall-Associated Virulence Factors Contribute to Increased Resilience of OldFrontiers in microbiology · 2019Article
- Antiphagocytic protein 1 increases the susceptibility of Cryptococcus neoformans to amphotericin B and fluconazole.PloS one · 2019Article
- Mechanisms of Pulmonary Escape and Dissemination by Cryptococcus neoformans.Journal of fungi (Basel, Switzerland) · 2018Review
- Cryptococcal pathogenic mechanisms: a dangerous trip from the environment to the brain.Memorias do Instituto Oswaldo Cruz · 2018Review
- The Crucial Role of Biofilms in Cryptococcus neoformans Survival within Macrophages and Colonization of the Central Nervous System.Journal of fungi (Basel, Switzerland) · 2017Review
- Control of Phagocytosis by Microbial Pathogens.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
In previous studies, we showed that the pathogenic fungus Cryptococcus neoformans (Cn) produces a specific and unique protein called antiphagocytic protein 1 (App1), which inhibits phagocytosis of Cn by alveolar macrophages (AMs). Phagocytosis of Cn by AMs occurs mainly through a complement- or Ab-mediated mechanism. Among AM receptors, complement receptor 3 (CR3) and FcRgamma are the most common receptors involved in the phagocytic process. Because App1 inhibits phagocytosis of complement- but not Ab-coated erythrocytes, we investigated the role of CR3 in App1-macrophage interactions. We found that App1 binds to CR3 and if CR3 is absent from the surface of AMs, its antiphagocytic action is lost. When we investigated whether App1 would also bind to other complement receptor(s), we found that App1 does bind to complement receptor 2 (CR2) in a dose-dependent manner. In certain lymphoma cell lines, cellular proliferation is stimulated by complement through CR2, providing a potential use of App1 as a proliferation inhibitor of these cells. Initially discovered as an antiphagocytic protein regulating CR3-mediated innate immunity, App1 may also play a key role in the regulation of acquired immunity, because CR2 is mainly localized on B cells.
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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.