ArticleMediators of inflammation2001
Role of ICAM-1 in the aggregation and adhesion of human alveolar macrophages in response to TNF-alpha and INF-gamma.
Article in Mediators of inflammation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Multiple Serum Cytokine Profiling to Identify Combinational Diagnostic Biomarkers in Attacks of Familial Mediterranean Fever.Medicine · 2016Trial
- Enlarged, activated alveolar macrophages as quantitative surrogates of disease activity in pulmonary sarcoidosis.Frontiers in medicine · 2026Article
- Signal regulating proteins (SIRPs) participate in sarcoidosis granuloma formation by promoting immune cell aggregation.Respiratory research · 2025Article
- Emerging Therapeutic Options for Refractory Pulmonary Sarcoidosis: The Evidence and Proposed Mechanisms of Action.Journal of clinical medicine · 2023Review
- Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19.PLoS genetics · 2022Article
- Transcriptome Analysis of Peripheral Blood Mononuclear Cells in Pulmonary Sarcoidosis.Frontiers in medicine · 2022Article
- Metabolic Programming of Macrophages: Implications in the Pathogenesis of Granulomatous Disease.Frontiers in immunology · 2019Review
- Granuloma formation in pulmonary sarcoidosis.Frontiers in immunology · 2013Review
- Uniocular anterior chamber inoculation of a tumor necrosis factor alpha-expressing recombinant of herpes simplex virus type 1 results in more rapid destruction and increased viral replication in the retina of the uninoculated eye.Journal of virology · 2008Article
- Tumor necrosis factor alpha and macrophages in the brain of herpes simplex virus type 1-infected BALB/c mice.Journal of neurovirology · 2006Article
- Intercellular adhesion molecule-1 is required for the early formation of granulomas and participates in the resistance of mice to the infection with the fungus Paracoccidioides brasiliensis.The American journal of pathology · 2006Article
Corrections and comments
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Authors and funding
10 authors.
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Abstract
Intracellular adhesion molecule-1 (ICAM-1)-mediated cell-cell adhesion is thought to play an important role at sites of inflammation. Recent evidence suggests that ICAM-1 surface expression on alveolar macrophages is increased in pulmonary sarcoidosis and that inflammatory granuloma formation is characterized by the aggregation of macrophages. The present study shows that ICAM-1 expression is significantly elevated on alveolar macrophages from patients with sarcoidosis in response to tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (INF-gamma) compared with healthy controls. Aggregation and adhesion were significantly increased in alveolar macrophages treated with TNF-alpha and INF-gamma, and significantly inhibited in those pretreated with a monoclonal antibody to ICAM-1. Similarly, aggregation and adhesion were inhibited in macrophages treated with heparin, which then exhibited a wide range of biological activities relevant to inflammation. These results suggested that the surface expression of ICAM-1 on alveolar macrophages in response to TNF-alpha and INF-gamma is important in mediating aggregation and adhesion. Additionally, heparin may be useful for developing novel therapeutic agents for fibrotic lung disease.
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