ArticleThe American journal of pathology2004
Human pulmonary fibroblasts exhibit altered interleukin-4 and interleukin-13 receptor subunit expression in idiopathic interstitial pneumonia.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Shared and unique transcriptomic signature genes and pathways among biopsy, peripheral blood mononuclear cells and bronchoalveolar lavage samples in IPF patients revealed using comparative meta-transcriptome analysis.Tuberkuloz ve toraks · 2024Pooled it
- A model for Crohn's disease post-ileal resection fibrosis development using human ileal enteroids and myofibroblasts.Frontiers in physiology · 2026Article
- Altered expression pattern of immune response-related genes and isoforms in hypersensitivity pneumonitis lung fibroblasts.Scientific reports · 2024Article
- Distinct fibroblast functions associated with fibrotic and immune-mediated inflammatory diseases and their implications for therapeutic development.F1000Research · 2024Review
- JAK/STAT pathway: Extracellular signals, diseases, immunity, and therapeutic regimens.Frontiers in bioengineering and biotechnology · 2023Review
- Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis.Molecules (Basel, Switzerland) · 2022Review
- Molecular Mechanisms and Physiological Changes behind Benign Tracheal and Subglottic Stenosis in Adults.International journal of molecular sciences · 2022Review
- Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms.International journal of molecular sciences · 2021Review
- Transcriptional regulation of the IL-13Rα2 gene in human lung fibroblasts.Scientific reports · 2020Article
- Inhibition of the stem cell factor 248 isoform attenuates the development of pulmonary remodeling disease.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Targeting MAP3K19 prevents human lung myofibroblast activation both in vitro and in a humanized SCID model of idiopathic pulmonary fibrosis.Scientific reports · 2019Article
- CCR10+ epithelial cells from idiopathic pulmonary fibrosis lungs drive remodeling.JCI insight · 2018Article
- Type 2 Immune Mechanisms in Carbon Nanotube-Induced Lung Fibrosis.Frontiers in immunology · 2018Review
- Type 2 immunity in tissue repair and fibrosis.Nature reviews. Immunology · 2018Review
- TRAIL-Dependent Resolution of Pulmonary Fibrosis.Mediators of inflammation · 2018Article
- Senescent stromal cell-induced divergence and therapeutic resistance in T cell acute lymphoblastic leukemia/lymphoma.Oncotarget · 2016Article
- Targeting interleukin-13 with tralokinumab attenuates lung fibrosis and epithelial damage in a humanized SCID idiopathic pulmonary fibrosis model.American journal of respiratory cell and molecular biology · 2014Article
- Protein kinase D is increased and activated in lung epithelial cells and macrophages in idiopathic pulmonary fibrosis.PloS one · 2014Article
- Deficient repair response of IPF fibroblasts in a co-culture model of epithelial injury and repair.Fibrogenesis & tissue repair · 2014Article
- STAT6 and lung inflammation.JAK-STAT · 2013Review
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Abnormal proliferation of pulmonary fibroblasts is a prominent feature of chronic pulmonary fibrotic diseases such as idiopathic interstitial pneumonia (IIP), but it is not presently clear how this proliferative response by lung fibroblasts can be therapeutically modulated. In the present study, we examined whether it was possible to selectively target primary human pulmonary fibroblasts grown out of surgical lung biopsies (SLBs) from IIP patients based on their expression of interleukin-4 receptor (IL-4R) and IL-13R subunits. Pulmonary fibroblast lines cultured from patients with the severest form of IIP, namely usual interstitial pneumonia, exhibited the greatest gene and protein expression of IL-4Ralpha, IL-13Ralpha1, and IL-13Ralpha2 compared with primary pulmonary fibroblast lines grown from other IIP SLBs and normal SLBs. When exposed to increasing concentrations of a chimeric protein comprised of human IL-13 and a truncated version of Pseudomonas exotoxin (IL13-PE), the proliferation of primary usual interstitial pneumonia fibroblasts was inhibited to a much greater extent compared with fibroblast lines from nonspecific interstitial pneumonia and respiratory bronchiolitis/interstitial lung disease patient groups. Fibroblasts from normal patients exhibited minimal susceptibility to the cytotoxic effect of IL13-PE. IL13-PE-mediated targeting of IIP fibroblasts was dependent on their expression of IL-4Ralpha and IL-13Ralpha2. Thus, these data suggest that the abnormal proliferative properties of human lung fibroblasts from certain IIP patient groups can be modulated in a manner that is dependent on the IL-4 and IL-13 receptor subunit expression by these cells.
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