ArticleHuman immunology2014
p38 Mitogen-Activated Protein Kinase in beryllium-induced dendritic cell activation.
Article in Human immunology, 2014. 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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The trial behind it
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Immune regulation by CD55 in chronic beryllium disease.American journal of respiratory cell and molecular biology · 2026Article
- Innate and Adaptive Immunity in Noninfectious Granulomatous Lung Disease.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- Proteomic characteristics of beryllium sulfate-induced differentially expressed proteins in rats.Toxicology research · 2021Article
- TLR9 and IL-1R1 Promote Mobilization of Pulmonary Dendritic Cells during Beryllium Sensitization.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Immunologic Effects of Beryllium Exposure.Annals of the American Thoracic Society · 2018Review
- Interplay of innate and adaptive immunity in metal-induced hypersensitivity.Current opinion in immunology · 2016Review
- Beryllium-induced lung disease exhibits expression profiles similar to sarcoidosis.The European respiratory journal · 2016Article
- Beryllium-Induced Hypersensitivity: Genetic Susceptibility and Neoantigen Generation.Journal of immunology (Baltimore, Md. : 1950) · 2016Review
- MyD88 dependence of beryllium-induced dendritic cell trafficking and CD4⁺ T-cell priming.Mucosal immunology · 2015Article
- Beryllium increases the CD14(dim)CD16+ subset in the lung of chronic beryllium disease.PloS one · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Dendritic cells (DC) play a role in the regulation of immune responses to haptens, which in turn impact DC maturation. Whether beryllium (Be) is able to induce DC maturation and if this occurs via the MAPK pathway is not known. Primary monocyte-derived DCs (moDCs) models were generated from Be non-exposed healthy volunteers as a non-sensitized cell model, while PBMCs from BeS (Be sensitized) and CBD (chronic beryllium disease) were used as disease models. The response of these cells to Be was evaluated. The expression of CD40 was increased significantly (p<0.05) on HLA-DP Glu69+ moDCs after 100 μM BeSO₄-stimulation. BeSO₄ induced p38MAPK phosphorylation, while IκB-α was degraded in Be-stimulated moDCs. The p38 MAPK inhibitor SB203580 blocked Be-induced NF-κB activation in moDCs, suggesting that p38MAPK and NF-κB are dependently activated by BeSO₄. Furthermore, in BeS and CBD subjects, SB203580 downregulated Be-stimulated proliferation in a dose-dependent manner, and decreased Be-stimulated TNF-α and IFNγ cytokine production. Taken together, this study suggests that Be-induces non-sensitized Glu69+ DCs maturation, and that p38MAPK signaling is important in the Be-stimulated DCs activation as well as subsequent T cell proliferation and cytokine production in BeS and CBD. In total, the MAPK pathway may serve as a potential therapeutic target for human granulomatous lung diseases.
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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.