ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Immunomodulation with IL-4R alpha antisense oligonucleotide prevents respiratory syncytial virus-mediated pulmonary disease.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 53 citations in OpenAlex.
- TLR4 genotype and environmental LPS mediate RSV bronchiolitis through Th2 polarization.The Journal of clinical investigation · 2015Trial
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- CD206Circulation · 2025Article
- Immune Checkpoint Inhibitors for Vaccine Improvements: Current Status and New Approaches.Pharmaceutics · 2022Review
- Neonatal Immune Responses to Respiratory Viruses.Frontiers in immunology · 2022Review
- Immune escaping of the novel genotypes of human respiratory syncytial virus based on gene sequence variation.Frontiers in immunology · 2022Article
- The role of goblet cells in viral pathogenesis.The FEBS journal · 2021Review
- Foxp3 Silencing with Antisense Oligonucleotide Improves Immunogenicity of an Adjuvanted Recombinant Vaccine againstInternational journal of molecular sciences · 2021Article
- Cytokine receptor clustering in sensory neurons with an engineered cytokine fusion protein triggers unique pain resolution pathways.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A model of respiratory syncytial virus (RSV) infection of infants in newborn lambs.Cell and tissue research · 2020Review
- Progress in the Use of Antisense Oligonucleotides for Vaccine Improvement.Biomolecules · 2020Review
- Contribution of Dendritic Cells in Protective Immunity against Respiratory Syncytial Virus Infection.Viruses · 2020Review
- Role of Type I Interferon (IFN) in the Respiratory Syncytial Virus (RSV) Immune Response and Disease Severity.Frontiers in immunology · 2019Review
- Neonatal Immunity, Respiratory Virus Infections, and the Development of Asthma.Frontiers in immunology · 2018Review
- The IL-4 receptor α has a critical role in bone marrow-derived fibroblast activation and renal fibrosis.Kidney international · 2017Article
- IL-4Rα on dendritic cells in neonates and Th2 immunopathology in respiratory syncytial virus infection.Journal of leukocyte biology · 2017Article
- Pulmonary Susceptibility of Neonates to Respiratory Syncytial Virus Infection: A Problem of Innate Immunity?Journal of immunology research · 2017Review
- Article
- Crawling with Virus: Translational Insights from a Neonatal Mouse Model on the Pathogenesis of Respiratory Syncytial Virus in Infants.Journal of virology · 2016Review
- Building a better neonatal mouse model to understand infant respiratory syncytial virus disease.Respiratory research · 2015Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Respiratory syncytial virus (RSV) causes significant morbidity and mortality in infants worldwide. Severe RSV infections in infants cause bronchiolitis, wheeze, and/or cough and significantly increase the risk for developing asthma. RSV pathogenesis is thought to be due to a Th2-type immune response initiated in response to RSV infection, specifically in the infant. Using a neonatal mouse system as an appropriate model for human infants, we sought to determine whether local inhibition of IL-4Rα expression during primary RSV infection in the neonate would prevent Th2-skewed responses to secondary RSV infection and improve long-term pulmonary function. To reduce IL-4Rα expression, antisense oligonucleotides (ASOs) specific for IL-4Rα were administered intranasally to neonatal mice at the time of primary infection. Mice were initially infected with RSV at 1 wk of age and were reinfected at 6 wk of age. Administration of IL-4Rα ASOs during primary RSV infection in neonatal mice abolished the pulmonary dysfunction normally observed following reinfection in the adult. This ablation of pulmonary dysfunction correlated with a persistent rebalancing of the Th cell compartment with decreased Th2 responses (i.e., reduced goblet cell hyperplasia, Th2 cells, and cytokine secretion) and increased Th1 responses (i.e., elevated Th1 cell numbers and type I Abs and cytokines). Our data support our hypothesis that a reduction in the Th2 immune response during primary infection in neonates prevents Th2-mediated pulmonary pathology initially and upon reinfection and further suggest that vaccine strategies incorporating IL-4Rα ASOs may be of significant benefit to infants.
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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.