ArticleAmerican journal of respiratory cell and molecular biology2021
Antifibrotics Modify B-Cell-induced Fibroblast Migration and Activation in Patients with Idiopathic Pulmonary Fibrosis.
Article in American journal of respiratory cell and molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.
- Transcriptomics of interstitial lung disease: a systematic review and meta-analysis.The European respiratory journal · 2025Pooled it
- Crosstalk between fibroblasts and immunocytes in fibrosis: From molecular mechanisms to clinical trials.Clinical and translational medicine · 2024Pooled it
- Recent advances in pulmonary fibrosis: from lung surfactant to the immune connection.Respiratory research · 2026Review
- Aberrant activation of tissue-resident lymphocytes and pro-fibrotic GZMK⁺ CD8⁺ T cells in IPF.Communications biology · 2026Article
- Tweaking the Complex Fibrogenic Role of Lymphocytes in Idiopathic Pulmonary Fibrosis.Tuberculosis and respiratory diseases · 2026Article
- Case-Based Immunology: B Cells and Systemic Sclerosis Interstitial Lung Disease.Arthritis & rheumatology (Hoboken, N.J.) · 2026Review
- Protein kinase C θ deletion ameliorates bleomycin-induced pulmonary fibrosis via the improvement of SIRT1/AMPK signaling on autophagy and senescence.Iranian journal of basic medical sciences · 2026Article
- Antifibrotic Strategies Targeting Phosphodiesterase-4 in Idiopathic Pulmonary Fibrosis: Molecular Mechanisms and Clinical Translation.Clinical pharmacology : advances and applications · 2026Review
- Target Fibroblast-B cell crosstalk via MIF signaling drives pathogenic B cell differentiation and joint damage in knee osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Transcriptomic Insights into Tumor Necrosis Factor α's Role in the Fibrosis-Related Processes of Equine Endometrial Fibroblasts.International journal of molecular sciences · 2025Article
- The crosstalk between autophagy and ferroptosis in pulmonary fibrosis.Journal of biomedical research · 2025Article
- Elucidating the role of IgA plasma cells and PECAM1-CD38 interaction in intestinal fibrosis: a single-cell RNA sequencing analysis in Crohn's disease.BMC gastroenterology · 2025Article
- Distinct lung functional, histological and cell senescence signatures in the single and repetitive bleomycin mouse models of idiopathic pulmonary fibrosis.Physiological reports · 2025Article
- Transcriptomic Features of Recurrence Rates in Idiopathic Subglottic Stenosis.The Laryngoscope · 2025Article
- Pirfenidone in Skin Fibrosis and Scarring: From Bench Insights to Clinical Data.Medical sciences (Basel, Switzerland) · 2025Review
- Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Dressed in Collagen: 2D and 3D Cardiac Fibrosis Models.International journal of molecular sciences · 2025Review
- Review
- Single Cell RNA-Seq Identifies Cell Subpopulations Contributing to Idiopathic Pulmonary Fibrosis in Humans.Journal of cellular and molecular medicine · 2025Article
- β-Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1.BMC immunology · 2025Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
B-cell activation is increasingly linked to numerous fibrotic lung diseases, and it is well known that aggregates of lymphocytes form in the lung of many of these patients. Activation of B-cells by pattern recognition receptors (PRRs) drives the release of inflammatory cytokines, chemokines, and metalloproteases important in the pathophysiology of pulmonary fibrosis. However, the specific mechanisms of B-cell activation in patients with idiopathic pulmonary fibrosis (IPF) are poorly understood. Herein, we have demonstrated that B-cell activation by microbial antigens contributes to the inflammatory and profibrotic milieu seen in patients with IPF. B-cell stimulation by CpG and β-glucan via PRRs resulted in activation of mTOR-dependent and independent pathways. Moreover, we showed that the B-cell-secreted inflammatory milieu is specific to the inducing antigen and causes differential fibroblast migration and activation. B-cell responses to infectious agents and subsequent B-cell-mediated fibroblast activation are modifiable by antifibrotics, but each seems to exert a specific and different effect. These results suggest that, upon PRR activation by microbial antigens, B-cells can contribute to the inflammatory and fibrotic changes seen in patients with IPF, and antifibrotics are able to at least partially reverse these responses.
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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.