ArticleFibrogenesis & tissue repair2011
TLR9-induced interferon β is associated with protection from gammaherpesvirus-induced exacerbation of lung fibrosis.
Article in Fibrogenesis & tissue repair, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Triple combination of interferon beta-1b, lopinavir-ritonavir, and ribavirin in the treatment of patients admitted to hospital with COVID-19: an open-label, randomised, phase 2 trial.Lancet (London, England) · 2020Trial
- Antifibrotic monocyte activation by nanoparticles resolves murine pulmonary fibrosis.Biomaterials · 2026Article
- Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2025Article
- Mitochondrial DNA Sensing Pathogen Recognition Receptors in Systemic Sclerosis Associated Interstitial Lung Disease: A Review.Current treatment options in rheumatology · 2023Article
- The innate and T-cell mediated immune response during acute and chronic gammaherpesvirus infection.Frontiers in cellular and infection microbiology · 2023Review
- Novaferon Effectively Inhibits Ancestral SARS-CoV-2 and Omicron VariantChina CDC weekly · 2022Article
- Activation and Evasion of Innate Immunity by Gammaherpesviruses.Journal of molecular biology · 2022Review
- Examination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis.Frontiers in immunology · 2022Review
- The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Promising Therapy for Heart Failure in Patients with Severe COVID-19: Calming the Cytokine Storm.Cardiovascular drugs and therapy · 2021Review
- Ontological modeling and analysis of experimentally or clinically verified drugs against coronavirus infection.Scientific data · 2021Article
- Evolving Perspectives on Innate Immune Mechanisms of IPF.Frontiers in molecular biosciences · 2021Review
- The Epithelial-Immune Crosstalk in Pulmonary Fibrosis.Frontiers in immunology · 2021Review
- Differential immune activation profile of SARS-CoV-2 and SARS-CoV infection in human lung and intestinal cells: Implications for treatment with IFN-β and IFN inducer.The Journal of infection · 2020Article
- PINK1 attenuates mtDNA release in alveolar epithelial cells and TLR9 mediated profibrotic responses.PloS one · 2019Article
- Recognition of Candida albicans by gingival fibroblasts: The role of TLR2, TLR4/CD14, and MyD88.Cytokine · 2018Article
- Innate Immunity in Systemic Sclerosis Fibrosis: Recent Advances.Frontiers in immunology · 2018Review
- The Role of Immune and Inflammatory Cells in Idiopathic Pulmonary Fibrosis.Frontiers in medicine · 2018Review
- Toll-like Receptor 9 Signaling Is Augmented in Systemic Sclerosis and Elicits Transforming Growth Factor β-Dependent Fibroblast Activation.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- Emerging roles of innate immune signaling and toll-like receptors in fibrosis and systemic sclerosis.Current rheumatology reports · 2015Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundWe have shown previously that murine gammaherpesvirus 68 (γHV68) infection exacerbates established pulmonary fibrosis. Because Toll-like receptor (TLR)-9 may be important in controlling the immune response to γHV68 infection, we examined how TLR-9 signaling effects exacerbation of fibrosis in response to viral infection, using models of bleomycin- and fluorescein isothiocyanate-induced pulmonary fibrosis in wild-type (Balb/c) and TLR-9-/- mice.
resultsWe found that in the absence of TLR-9 signaling, there was a significant increase in collagen deposition following viral exacerbation of fibrosis. This was not associated with increased viral load in TLR-9-/- mice or with major alterations in T helper (Th)1 and Th2 cytokines. We examined alveolar epithelial-cell apoptosis in both strains, but this could not explain the altered fibrotic outcomes. As expected, TLR-9-/- mice had a defect in the production of interferon (IFN)-β after viral infection. Balb/c fibroblasts infected with γHV68 in vitro produced more IFN-β than did infected TLR-9-/- fibroblasts. Accordingly, in vitro infection of Balb/c fibroblasts resulted in reduced proliferation rates whereas infection of TLR-9-/- fibroblasts did not. Finally, therapeutic administration of CpG oligodeoxynucleotides ameliorated bleomycin-induced fibrosis in wild-type mice.
conclusionsThese results show a protective role for TLR-9 signaling in murine models of lung fibrosis, and highlight differences in the biology of TLR-9 between mice and humans.
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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.