ArticleMediators of inflammation2003
Expression of Fas antigen and Fas ligand in bronchoalveolar lavage from silicosis patients.
Article in Mediators of inflammation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 13 citations in OpenAlex.
- The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis.International journal of molecular sciences · 2021Review
- Immunity to the Dual Threat of Silica Exposure andFrontiers in immunology · 2018Review
- An overview of caspase: Apoptotic protein for silicosis.Indian journal of occupational and environmental medicine · 2010Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo understand the role of apoptosis through Fas/Fas ligand (FasL) interaction in the pathogenesis of silicosis, we examined the expression of Fas antigen, FasL and apoptosis in bronchoalveolar lavage fluid lymphocytes obtained from patients with silicosis. MATERIALS AND
methodsTen patients with silicosis, and 10 healthy controls were studied. Non-adherent cells were separated and analysed by cytometry for the expression of Fas antigen, FasL, and the co-expression of Fas/FasL. By double staining, we studied the FasL expression on CD4, CD8, CD56 and CD45RO-positive cells. DNA fragmentation was investigated by the terminal deoxy(d) UTP nick end labelling (TUNEL) method.
resultsWe have found Fas and FasL expression in silicosis patients to be significantly higher than those in healthy controls. Interestingly, 6-18% of lymphocytes from silicosis patients co-expressed Fas and FasL. In silicosis patients, FasL was highly expressed on CD4+, CD56+ and CD45RO+ bronchoalveolar lavage cells. Fas antigen expressing cells showed DNA fragmentation characteristic for apoptosis.
conclusionFasL was significantly expressed on cytotoxic effector and memory cells. The Fas/FasL system is implicated in the inflammatory process observed in silicosis patients.
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