ArticlePLoS pathogens2016
An Epithelial Integrin Regulates the Amplitude of Protective Lung Interferon Responses against Multiple Respiratory Pathogens.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 46 citations in OpenAlex.
- TGFβ primes alveolar-like macrophages to induce type I IFN following TLR2 activation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Orchestrating immunopathology: the spectrum of programmed cell death pathways co-opted by influenza a virus in pulmonary immunity.Frontiers in immunology · 2026Review
- Diet switch pre-vaccination improves immune response and metabolic status in formerly obese mice.Nature microbiology · 2024Article
- Low level of tonic interferon signalling is associated with enhanced susceptibility to SARS-CoV-2 variants of concern in human lung organoids.Emerging microbes & infections · 2023Article
- Alveolar macrophages in tissue homeostasis, inflammation, and infection: evolving concepts of therapeutic targeting.The Journal of clinical investigation · 2023Review
- COVID-19 in Patients with Chronic Lung Disease.Clinics in chest medicine · 2023Review
- After the Storm: Regeneration, Repair, and Reestablishment of Homeostasis Between the Alveolar Epithelium and Innate Immune System Following Viral Lung Injury.Annual review of pathology · 2023Review
- Biology of lung macrophages in health and disease.Immunity · 2022Review
- Receptor binding domain of SARS-CoV-2 is a functional αv-integrin agonist.bioRxiv : the preprint server for biology · 2022Article
- Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity.Nature communications · 2021Article
- Influenza virus and SARS-CoV-2: pathogenesis and host responses in the respiratory tract.Nature reviews. Microbiology · 2021Review
- COVID-19 and pulmonary fibrosis: A potential role for lung epithelial cells and fibroblasts.Immunological reviews · 2021Review
- GP96 Drives Exacerbation of Secondary Bacterial Pneumonia following Influenza A Virus Infection.mBio · 2021Article
- Reply to AlthuwaybiAmerican journal of respiratory and critical care medicine · 2021Article
- Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity.bioRxiv : the preprint server for biology · 2021Article
- Influenza in High-Risk Hosts-Lessons Learned from Animal Models.Cold Spring Harbor perspectives in medicine · 2020Review
- Demystifying pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Pulmonary fibrosis and COVID-19: the potential role for antifibrotic therapy.The Lancet. Respiratory medicine · 2020Review
- Regulation of barrier immunity and homeostasis by integrin-mediated transforming growth factor β activation.Immunology · 2020Review
- Target the Host, Kill the Bug; Targeting Host Respiratory Immunosuppressive Responses as a Novel Strategy to Improve Bacterial Clearance During Lung Infection.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
21 authors at 3 institutions in 2 countries.
Funding
Abstract
The healthy lung maintains a steady state of immune readiness to rapidly respond to injury from invaders. Integrins are important for setting the parameters of this resting state, particularly the epithelial-restricted αVβ6 integrin, which is upregulated during injury. Once expressed, αVβ6 moderates acute lung injury (ALI) through as yet undefined molecular mechanisms. We show that the upregulation of β6 during influenza infection is involved in disease pathogenesis. β6-deficient mice (β6 KO) have increased survival during influenza infection likely due to the limited viral spread into the alveolar spaces leading to reduced ALI. Although the β6 KO have morphologically normal lungs, they harbor constitutively activated lung CD11b+ alveolar macrophages (AM) and elevated type I IFN signaling activity, which we traced to the loss of β6-activated transforming growth factor-β (TGF-β). Administration of exogenous TGF-β to β6 KO mice leads to reduced numbers of CD11b+ AMs, decreased type I IFN signaling activity and loss of the protective phenotype during influenza infection. Protection extended to other respiratory pathogens such as Sendai virus and bacterial pneumonia. Our studies demonstrate that the loss of one epithelial protein, αVβ6 integrin, can alter the lung microenvironment during both homeostasis and respiratory infection leading to reduced lung injury and improved survival.
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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.