ReviewAdvances in immunology2009
Immune pathways for translating viral infection into chronic airway disease.
Review in Advances in immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 46 citations in OpenAlex.
- Respiratory Syncytial Virus-Specific Antibodies and Atopic Diseases in Children: A 10-Year Follow-Up.Pathogens (Basel, Switzerland) · 2023Article
- SARS-CoV-2 infection of airway cells causes intense viral and cell shedding, two spreading mechanisms affected by IL-13.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Lung epithelial cells: therapeutically inducible effectors of antimicrobial defense.Mucosal immunology · 2018Review
- The Metabolic Prospective and Redox Regulation of Macrophage Polarization.Journal of clinical & cellular immunology · 2015Article
- Protective effect of a Protein Epitope Mimetic CCR10 antagonist, POL7085, in a model of allergic eosinophilic airway inflammation.Respiratory research · 2015Article
- The microbiome in asthma.The Journal of allergy and clinical immunology · 2015Review
- Perinatal and early childhood environmental factors influencing allergic asthma immunopathogenesis.International immunopharmacology · 2014Review
- Double-stranded RNA induces molecular and inflammatory signatures that are directly relevant to COPD.Mucosal immunology · 2013Article
- The role of early life viral bronchiolitis in the inception of asthma.Current opinion in allergy and clinical immunology · 2013Review
- Probiotics in the management of lung diseases.Mediators of inflammation · 2013Review
- Airway smooth muscle STIM1 and Orai1 are upregulated in asthmatic mice and mediate PDGF-activated SOCE, CRAC currents, proliferation, and migration.Pflugers Archiv : European journal of physiology · 2012Article
- Role of TNFR1 in the innate airway hyperresponsiveness of obese mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Respiratory viral infections in children with asthma: do they matter and can we prevent them?BMC pediatrics · 2012Article
- The influence of virus infections on the course of COPD.European journal of microbiology & immunology · 2012Review
- T inflammatory memory CD8 T cells participate to antiviral response and generate secondary memory cells with an advantage in XCL1 production.Immunologic research · 2012Article
- Interleukin-25 induces type 2 cytokine production in a steroid-resistant interleukin-17RB+ myeloid population that exacerbates asthmatic pathology.Nature medicine · 2012Article
- Review
- Host epithelial-viral interactions as cause and cure for asthma.Current opinion in immunology · 2011Review
- Airway mucus function and dysfunction.The New England journal of medicine · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
To better understand the immune basis for chronic inflammatory lung disease, we analyzed a mouse model of lung disease that develops after respiratory viral infection. The disease that develops in this model is similar to asthma and chronic obstructive pulmonary disease (COPD) in humans and is manifested after the inciting virus has been cleared to trace levels. The model thereby mimics the relationship of paramyxoviral infection to the development of childhood asthma in humans. When the acute lung disease appears in this model (at 3 weeks after viral inoculation), it depends on an immune axis that is initiated by expression and activation of the high-affinity IgE receptor (FcvarepsilonRI) on conventional lung dendritic cells (cDCs) to recruit interleukin (IL)-13-producing CD4(+) T cells to the lower airways. However, when the chronic lung disease develops fully (at 7 weeks after inoculation), it is driven instead by an innate immune axis that relies on invariant natural killer T (iNKT) cells that are programmed to activate macrophages to produce IL-13. The interaction between iNKT cells and macrophages depends on contact between the semi-invariant Valpha14Jalpha18-TCR on lung iNKT cells and the oligomorphic MHC-like protein CD1d on macrophages as well as NKT cell production of IL-13 that binds to the IL-13 receptor (IL-13R) on the macrophage. This innate immune axis is also activated in the lungs of humans with severe asthma or COPD based on detection of increased numbers of iNKT cells and alternatively activated IL-13-producing macrophages in the lung. Together, the findings identify an adaptive immune response that mediates acute disease and an innate immune response that drives chronic inflammatory lung disease in experimental and clinical settings.
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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.