ArticleMedical science monitor : international medical journal of experimental and clinical research2021
Regulatory Effect of PD1/PD-Ligand 1 (PD-L1) on Treg Cells in Patients with Idiopathic Pulmonary Fibrosis.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Global Trends in Hepatocellular Carcinoma and TGF-β Research: A Bibliometric and Visualization Analysis from 2000 to 2024.Current protein & peptide science · 2026Article
- Reprogrammed Fibrotic Niche Fuels Lung Cancer Initiation and Reciprocal Remodeling.International journal of biological sciences · 2026Review
- CD4Frontiers in immunology · 2025Review
- Tissue-specific roles of regulatory T cells: mechanisms of suppression and beyond along with emerging therapeutic insights in autoimmune indications.Frontiers in immunology · 2025Review
- Inhibitor of PD-1/PD-L1: a new approach may be beneficial for the treatment of idiopathic pulmonary fibrosis.Journal of translational medicine · 2024Review
- Integrated analysis reveals crosstalk between pyroptosis and immune regulation in renal fibrosis.Frontiers in immunology · 2024Article
- Updates on the controversial roles of regulatory lymphoid cells in idiopathic pulmonary fibrosis.Frontiers in immunology · 2024Review
- Evaluation of PD-1 T lymphocytes in bronchoalveolar lavage in lung cancer compared to benign lung diseases.Clinical and experimental medicine · 2023Article
- Regulatory T cells in lung disease and transplantation.Bioscience reports · 2023Review
- T cells in idiopathic pulmonary fibrosis: crucial but controversial.Cell death discovery · 2023Review
- PD-1 and PD-L1: architects of immune symphony and immunotherapy breakthroughs in cancer treatment.Frontiers in immunology · 2023Review
- What role does PDL1 play in EMT changes in tumors and fibrosis?Frontiers in immunology · 2023Review
- The role of PD-1/PD-L1 axis in idiopathic pulmonary fibrosis: Friend or foe?Frontiers in immunology · 2022Review
- Transcriptome Classification Reveals Molecular Subgroups in Idiopathic Pulmonary Fibrosis.Genetics research · 2022Article
- Soluble Programmed Death Ligand-1 (sPD-L1): A Pool of Circulating Proteins Implicated in Health and Diseases.Cancers · 2021Review
- Immune Stroma in Lung Cancer and Idiopathic Pulmonary Fibrosis: A Common Biologic Landscape?International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Idiopathic pulmonary fibrosis (IPF) is a serious irreversible lung disease. The mechanism of immune checkpoint in idiopathic pulmonary fibrosis is still unknown. MATERIAL AND METHODS First, the expression levels of PD-1/PD-L1 on the surface of CD4+ T cells and the proportion of Treg cells in IPF or controls were detected by flow cytometry. Then, expression of TGF-ß in blood samples was detected with ELISA. Moreover, a co-culture system was composed of fibroblasts stimulated by TGF-ß and CD4+ T cells from healthy people. The proportions of Treg cells and PD-1 in the co-culture system were detected. In addition, we detected the proportion of Treg cells and the level of collagen-1 after adding PD-1 or PD-L1 protein antibody blocker to the co-culture system. RESULTS Flow cytometry revealed the upregulated expression of PD-1/PD-L1 in CD4+ T cells of IPF patients. PD-1 appears to inhibit the differentiation of CD4+ T cells into Treg cells. Co-culture of myofibroblasts and CD4+ T cells induced the generation of collagen-1 and reduced the proliferation of CD4+ T cells. When PD-1 was blocked, the inhibition of Treg cell differentiation was reversed, accompanied by decreased collagen-1 production. CONCLUSIONS This work identified the molecular mechanism of PD-1 in patients with IPF. It may provide a new perspective on the therapeutic effect of PD-1.
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