ArticleFrontiers in pharmacology2014
CD4+CD25+FoxP3+ Regulatory Tregs inhibit fibrocyte recruitment and fibrosis via suppression of FGF-9 production in the TGF-β1 exposed murine lung.
Article in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Immune cells in keloids: mechanisms and potential treatments.Annals of medicine · 2026Review
- Oncogenic Kras targeting with MRTX1133 or Daraxonrasib specifically synergize with anti-CTLA4 to promote anti-tumor immunity in pancreatic cancer.Nature communications · 2026Article
- The transcriptome of CD14The European respiratory journal · 2026Article
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- An intricate relationship between fibrosis and autoimmune diseases: a specific focus on unraveling its molecular, immunological, and epigenetic drivers.Frontiers in immunology · 2026Review
- CAR-engineered cytolytic Tregs reverse pulmonary fibrosis and remodel the fibrotic niche with limited CRS.JCI insight · 2025Article
- Identifying TNFSF4Stem cell research & therapy · 2025Article
- The role of immune cells and inflammation in pulmonary hypertension: mechanisms and implications.Frontiers in immunology · 2024Review
- Allies or enemies? The effect of regulatory T cells and related T lymphocytes on the profibrotic environment in bleomycin-injured lung mouse models.Clinical and experimental medicine · 2023Review
- Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023Article
- Identification of immune biomarkers associated with basement membranes in idiopathic pulmonary fibrosis and their pan-cancer analysis.Frontiers in genetics · 2023Article
- Construction of prediction model of inflammation related genes in idiopathic pulmonary fibrosis and its correlation with immune microenvironment.Frontiers in immunology · 2022Article
- Identification of diagnostic gene biomarkers related to immune infiltration in patients with idiopathic pulmonary fibrosis based on bioinformatics strategies.Frontiers in medicine · 2022Article
- Inflammation in Pulmonary Arterial Hypertension.Advances in experimental medicine and biology · 2021Review
- Regulatory Immune Cells in Idiopathic Pulmonary Fibrosis: Friends or Foes?Frontiers in immunology · 2021Review
- Pulmonary toxicants and fibrosis: innate and adaptive immune mechanisms.Toxicology and applied pharmacology · 2020Review
- A Question of Tolerance-Antigen-Specific Immunotherapy for Type 1 Diabetes.Current diabetes reports · 2020Review
- Tolerogenic vaccines: Targeting the antigenic and cytokine niches of FOXP3Cellular immunology · 2020Review
- The Roles of Immune Cells in the Pathogenesis of Fibrosis.International journal of molecular sciences · 2020Review
- The Role of Regulatory T Cells in Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2019Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Pulmonary fibrosis is a difficult to treat, often fatal disease whose pathogenesis involves dysregulated TGF-β1 signaling. CD4+CD25+FoxP3+ Regulatory T cells ("Tregs") exert important effects on host tolerance and arise from naïve CD4+ lymphocytes in response to TGF-β1. However, the precise contribution of Tregs to experimentally induced murine lung fibrosis remains unclear. We sought to better understand the role of Tregs in this context. Using a model of fibrosis caused by lung specific, doxycycline inducible overexpression of the bioactive form of the human TGF-β1 gene we find that Tregs accumulate in the lung parenchyma within 5 days of transgene activation and that this enhancement persists to at least 14 days. Anti-CD25 Antibody mediated depletion of Tregs causes increased accumulation of soluble collagen and of intrapulmonary CD45+Col Iα1 fibrocytes. These effects are accompanied by enhanced local concentrations of the classical inflammatory mediators CD40L, TNF-α, and IL-1α, along with the neuroimmune molecule fibroblast growth factor 9 (FGF-9, also known as "glial activating factor"). FGF-9 expression localizes to parenchymal cells and alveolar macrophages in this model and antibody mediated neutralization of FGF-9 results in attenuated detection of intrapulmonary collagen and fibrocytes without affecting Treg quantities. These data indicate that CD4+CD25+FoxP3+ Tregs attenuate TGF-β1 induced lung fibrosis and fibrocyte accumulation in part via suppression of FGF-9.
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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.