ArticleFrontiers in immunology2018
4-1BB Signaling Promotes Alveolar Macrophages-Mediated Pro-Fibrotic Responses and Crystalline Silica-Induced Pulmonary Fibrosis in Mice.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The KLF4-inflammatory pathway is associated with paraquat-induced pulmonary injury and early pro-fibrotic responses.Biochemistry and biophysics reports · 2026Article
- Cholesterol-mediated inflammation activation in alveolar macrophages.BMC biology · 2025Article
- Global scenario of silica-associated diseases: A review on emerging pathophysiology of silicosis and potential therapeutic regimes.Toxicology reports · 2025Review
- Yangqing Chenfei formula alleviates crystalline silica induced pulmonary inflammation and fibrosis by suppressing macrophage polarization.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis.Frontiers in immunology · 2021Review
- Article
- Dioscin Alleviates Crystalline Silica-Induced Pulmonary Inflammation and Fibrosis through Promoting Alveolar Macrophage Autophagy.Theranostics · 2019Article
- CD137L-DCs, Potent Immune-Stimulators-History, Characteristics, and Perspectives.Frontiers in immunology · 2019Review
- OX40 (CD134) and OX40 ligand, important immune checkpoints in cancer.OncoTargets and therapy · 2019Article
- Dihydrotanshinone I Alleviates Crystalline Silica-Induced Pulmonary Inflammation by Regulation of the Th Immune Response and Inhibition of STAT1/STAT3.Mediators of inflammation · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silicosis is caused by exposure to crystalline silica (CS). We have previously shown that blocking 4-1BB signaling attenuated CS-induced inflammation and pulmonary fibrosis. However, the cells that express 4-1BB, which plays a vital role in promoting fibrosis, are still unknown. In this study, we demonstrated that the expression of 4-1BB is elevated in alveolar macrophages (AMs) in the lungs of CS-injured mice. CS exposure also markedly enhanced the expression of 4-1BB in macrophage-like, MH-S cells. In these cells, activation of the 4-1BB signaling with an agonist antibody led to upregulated secretion of pro-fibrotic mediators. Consistently, blocking 4-1BB downstream signaling or genetic deletion of 4-1BB alleviated pro-fibrotic responses
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