ArticleImmunology2016
Contribution of Fcγ receptors to human respiratory syncytial virus pathogenesis and the impairment of T-cell activation by dendritic cells.
Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 29 citations in OpenAlex.
- Preclinical characterisation of the protective capacity of an anti-nucleoprotein hRSV monoclonal antibody.EBioMedicine · 2026Article
- Analysis of BeyfortusCurrent issues in molecular biology · 2024Review
- Antibody-Dependent Enhancement (ADE) and the role of complement system in disease pathogenesis.Molecular immunology · 2022Review
- Cell surface detection of vimentin, ACE2 and SARS-CoV-2 Spike proteins reveals selective colocalization at primary cilia.Scientific reports · 2022Article
- Building a better antibody through the Fc: advances and challenges in harnessing antibody Fc effector functions for antiviral protection.Human vaccines & immunotherapeutics · 2021Review
- Article
- Lung pathology due to hRSV infection impairs blood-brain barrier permeability enabling astrocyte infection and a long-lasting inflammation in the CNS.Brain, behavior, and immunity · 2021Article
- Contribution of NKT cells to the immune response and pathogenesis triggered by respiratory viruses.Virulence · 2020Article
- Innate Immune Components that Regulate the Pathogenesis and Resolution of hRSV and hMPV Infections.Viruses · 2020Review
- Fcγ Receptor IIaFrontiers in cellular and infection microbiology · 2020Article
- Respiratory Syncytial Virus Infects Primary Neonatal and Adult Natural Killer Cells and Affects Their Antiviral Effector Function.The Journal of infectious diseases · 2019Article
- Article
- Immune-Modulation by the Human Respiratory Syncytial Virus: Focus on Dendritic Cells.Frontiers in immunology · 2019Review
- Contribution of Fcγ Receptor-Mediated Immunity to the Pathogenesis Caused by the Human Respiratory Syncytial Virus.Frontiers in cellular and infection microbiology · 2019Review
- Fc-Mediated Antibody Effector Functions During Respiratory Syncytial Virus Infection and Disease.Frontiers in immunology · 2019Review
- Article
- Functional Impairment of Mononuclear Phagocyte System by the Human Respiratory Syncytial Virus.Frontiers in immunology · 2017Review
- Characteristics of RSV-Specific Maternal Antibodies in Plasma of Hospitalized, Acute RSV Patients under Three Months of Age.PloS one · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human respiratory syncytial virus (hRSV) is the leading cause of infant hospitalization related to respiratory disease. Infection with hRSV produces abundant infiltration of immune cells into the airways, which combined with an exacerbated pro-inflammatory immune response can lead to significant damage to the lungs. Human RSV re-infection is extremely frequent, suggesting that this virus may have evolved molecular mechanisms that interfere with host adaptive immunity. Infection with hRSV can be reduced by administering a humanized neutralizing antibody against the virus fusion protein in high-risk infants. Although neutralizing antibodies against hRSV effectively block the infection of airway epithelial cells, here we show that both, bone marrow-derived dendritic cells (DCs) and lung DCs undergo infection with IgG-coated virus (hRSV-IC), albeit abortive. Yet, this is enough to negatively modulate DC function. We observed that such a process is mediated by Fcγ receptors (FcγRs) expressed on the surface of DCs. Remarkably, we also observed that in the absence of hRSV-specific antibodies FcγRIII knockout mice displayed significantly less cellular infiltration in the lungs after hRSV infection, compared with wild-type mice, suggesting a potentially harmful, IgG-independent role for this receptor in hRSV disease. Our findings support the notion that FcγRs can contribute significantly to the modulation of DC function by hRSV and hRSV-IC. Further, we provide evidence for an involvement of FcγRIII in the development of hRSV pathogenesis.
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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.