ArticleHistochemistry and cell biology2008
TLR9 is expressed in idiopathic interstitial pneumonia and its activation promotes in vitro myofibroblast differentiation.
Article in Histochemistry and cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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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Who cites it
35 citing papers in PubMed, 61 citations in OpenAlex.
- 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
- Attenuation of Pulmonary Fibrosis by the MyD88 Inhibitor TJ-M2010-5 Through Autophagy Induction in Mice.Biomedicines · 2025Article
- Mitochondrial DNA Sensing Pathogen Recognition Receptors in Systemic Sclerosis Associated Interstitial Lung Disease: A Review.Current treatment options in rheumatology · 2023Article
- Prevention of bleomycin-induced pulmonary fibrosis by a RANKL peptide in mice.Scientific reports · 2022Article
- Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2021Review
- Therapeutic Effect of Neuraminidase-1-Selective Inhibition in Mouse Models of Bleomycin-Induced Pulmonary Inflammation and Fibrosis.The Journal of pharmacology and experimental therapeutics · 2021Article
- Interstitial Lung Disease in Connective Tissue Disease: A Common Lesion With Heterogeneous Mechanisms and Treatment Considerations.Frontiers in immunology · 2021Review
- The Epithelial-Immune Crosstalk in Pulmonary Fibrosis.Frontiers in immunology · 2021Review
- More than a Genetic Code: Epigenetics of Lung Fibrosis.Molecular diagnosis & therapy · 2020Review
- Mitochondrial quality control in pulmonary fibrosis.Redox biology · 2020Review
- Targeting MAP3K19 prevents human lung myofibroblast activation both in vitro and in a humanized SCID model of idiopathic pulmonary fibrosis.Scientific reports · 2019Article
- PINK1 attenuates mtDNA release in alveolar epithelial cells and TLR9 mediated profibrotic responses.PloS one · 2019Article
- Targeting of TAM Receptors Ameliorates Fibrotic Mechanisms in Idiopathic Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2018Article
- Microbes Are Associated with Host Innate Immune Response in Idiopathic Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2017Article
- Heterogeneity of Fibroblasts and Myofibroblasts in Pulmonary Fibrosis.Current pathobiology reports · 2017Article
- Toll-like receptor 9 prevents cardiac rupture after myocardial infarction in mice independently of inflammation.American journal of physiology. Heart and circulatory physiology · 2016Article
- Elevated expression of NEU1 sialidase in idiopathic pulmonary fibrosis provokes pulmonary collagen deposition, lymphocytosis, and fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- The macrophages in rheumatic diseases.Journal of inflammation research · 2016Review
- Fibrosis--a lethal component of systemic sclerosis.Nature reviews. Rheumatology · 2014Review
- Beyond the genome: epigenetic mechanisms in lung remodeling.Physiology (Bethesda, Md.) · 2014Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Infectious diseases can be cofactors in idiopathic interstitial pneumonias (IIP) pathogenesis; recent data suggests that toll-like receptors 9 (TLR9) ligands contribute to experimental chronic tissue remodeling. Real-time TAQMAN and immunohistochemical analysis of IIP normal surgical lung biopsies (SLBs), primary fibroblast lines grown from both IIP and normal SLBs indicate that TLR9 is prominently and differentially expressed in a disease-specific manner. TLR9 expression was increased in biopsies from patients with IIP compared with normal lung biopsies and its expression is localized to areas of marked interstitial fibrosis. TLR9 in fibroblasts appeared to be increased by profibrotic Th2 cytokines (IL-4 and IL-13) and this was true in fibroblasts cultured from the most severe form of IIP, idiopathic pulmonary fibrosis (IPF) SLBs, in non-specific interstitial pneumonia fibroblast lines, and in normal fibroblasts. Finally, confocal microscopy studies have shown that TLR9 activation by its synthetic agonist CpG-ODN significantly increased the expression of alpha smooth muscle actin, the main marker of myofibroblast differentiation. These data indicate that TLR9 expression may drive the abnormal tissue healing response in severe forms of IIP and its activation can have a key role in myofibroblast differentiation promoting the progression of disease during the terminal phase of IPF.
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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.