ArticleScience translational medicine2010
TLR9 differentiates rapidly from slowly progressing forms of idiopathic pulmonary fibrosis.
Article in Science translational medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
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The trial behind it
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Who cites it
91 citing papers in PubMed, 161 citations in OpenAlex.
- Mechanosignaling through YAP and TAZ drives fibroblast activation and fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2015Trial
- Lung microbiome and disease progression in idiopathic pulmonary fibrosis: an analysis of the COMET study.The Lancet. Respiratory medicine · 2014Trial
- Fibroblast proliferative capacity predicts prognosis in idiopathic pulmonary fibrosis and identifies PITX1 as a growth-associated gene.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026Article
- Monocyte-mediated mechanisms in idiopathic pulmonary fibrosis: opportunities for early intervention.Apoptosis : an international journal on programmed cell death · 2026Review
- Epithelial damage and ageing: the perfect storm.Thorax · 2025Review
- Cyclic GMP-AMP synthase expression is enhanced in systemic sclerosis-associated interstitial lung disease and stimulates inflammatory myofibroblast activation.The European respiratory journal · 2025Article
- CD103+ dendritic cell-fibroblast crosstalk via TLR9, TDO2, and AHR signaling drives lung fibrogenesis.JCI insight · 2025Article
- A novel mouse model of myositis-associated interstitial lung disease was established by using TLR9 agonist combined with muscle homogenate.Clinical and experimental immunology · 2025Article
- Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2025Article
- Plasmacytoid Dendritic Cells Mediate CpG-ODN-induced Increase in Survival in a Mouse Model of Lymphangioleiomyomatosis.American journal of respiratory cell and molecular biology · 2024Article
- TLR9 activation in large wound induces tissue repair and hair follicle regeneration via γδT cells.Cell death & disease · 2024Article
- Pharmacological treatment in Idiopathic Pulmonary Fibrosis: current issues and future perspectivesMultidisciplinary respiratory medicine · 2024Article
- Plasmacytoid dendritic cells mediate CpG-ODN induced increase in survival in a mouse model of lymphangioleiomyomatosis.bioRxiv : the preprint server for biology · 2024Article
- Article
- Mitochondrial DNA Sensing Pathogen Recognition Receptors in Systemic Sclerosis Associated Interstitial Lung Disease: A Review.Current treatment options in rheumatology · 2023Article
- Translational Studies Reveal the Divergent Effects of Simtuzumab Targeting LOXL2 in Idiopathic Pulmonary Fibrosis.Fibrosis (Hong Kong, China) · 2023Article
- Article
- Time-course transcriptome analysis of a double challenge bleomycin-induced lung fibrosis rat model uncovers ECM homoeostasis-related translationally relevant genes.BMJ open respiratory research · 2023Article
- Prostaglandin E2 (PGE2) and Roflumilast Involvement in IPF Progression.International journal of molecular sciences · 2023Review
- Genetic variations in idiopathic pulmonary fibrosis and patient response to pirfenidone.Heliyon · 2023Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis is characterized by diffuse alveolar damage and severe fibrosis, resulting in a steady worsening of lung function and gas exchange. Because idiopathic pulmonary fibrosis is a generally progressive disorder with highly heterogeneous disease progression, we classified affected patients as either rapid or slow progressors over the first year of follow-up and then identified differences between the two groups to investigate the mechanism governing rapid progression. Previous work from our laboratory has demonstrated that Toll-like receptor 9 (TLR9), a pathogen recognition receptor that recognizes unmethylated CpG motifs in bacterial and viral DNA, promotes myofibroblast differentiation in lung fibroblasts cultured from biopsies of patients with idiopathic pulmonary fibrosis. Therefore, we hypothesized that TLR9 functions as both a sensor of pathogenic molecules and a profibrotic signal in rapidly progressive idiopathic pulmonary fibrosis. Indeed, TLR9 was present at higher concentrations in surgical lung biopsies from rapidly progressive patients than in tissue from slowly progressing patients. Moreover, fibroblasts from rapid progressors were more responsive to the TLR9 agonist, CpG DNA, than were fibroblasts from slowly progressing patients. Using a humanized severe combined immunodeficient mouse, we then demonstrated increased fibrosis in murine lungs receiving human lung fibroblasts from rapid progressors compared with mice receiving fibroblasts from slowly progressing patients. This fibrosis was exacerbated by intranasal CpG challenges. Furthermore, CpG induced the differentiation of blood monocytes into fibrocytes and the epithelial-to-mesenchymal transition of A549 lung epithelial cells. These data suggest that TLR9 may drive the pathogenesis of rapidly progressive idiopathic pulmonary fibrosis and may serve as a potential indicator for this subset of the disease.
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What OpenQuestion holds
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.