ArticleThe Journal of clinical investigation1995
Activation of the Fas receptor on lung eosinophils leads to apoptosis and the resolution of eosinophilic inflammation of the airways.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 156 citations in OpenAlex.
- Apoptosis of Eosinophil Granulocytes.Biology · 2020Review
- Apoptotic Cell-Directed Resolution of Lung Inflammation Requires Myeloid αv Integrin-Mediated Induction of Regulatory T Lymphocytes.The American journal of pathology · 2020Article
- DP1 receptor signaling prevents the onset of intrinsic apoptosis in eosinophils and functions as a transcriptional modulator.Journal of leukocyte biology · 2018Article
- OK-432 Acts as Adjuvant to Modulate T Helper 2 Inflammatory Responses in a Murine Model of Asthma.Journal of immunology research · 2018Article
- Myeloid Cells in Asthma.Microbiology spectrum · 2017Review
- Determinants of eosinophil survival and apoptotic cell death.Apoptosis : an international journal on programmed cell death · 2015Review
- Pin1-FADD interactions regulate Fas-mediated apoptosis in activated eosinophils.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Systemic FasL neutralization increases eosinophilic inflammation in a mouse model of asthma.Allergy · 2012Article
- Resolution of allergic airway inflammation and airway hyperreactivity is mediated by IL-17-producing {gamma}{delta}T cells.American journal of respiratory and critical care medicine · 2010Article
- Resolution of cell-mediated airways diseases.Respiratory research · 2010Review
- The role of costimulatory molecules in allergic disease and asthma.International archives of allergy and immunology · 2010Review
- Origin, regulation and physiological function of intestinal oeosinophils.Best practice & research. Clinical gastroenterology · 2008Review
- Fas-positive T cells regulate the resolution of airway inflammation in a murine model of asthma.The Journal of experimental medicine · 2006Article
- Effects of steroid treatment on lung CC chemokines, apoptosis and transepithelial cell clearance during development and resolution of allergic airway inflammation.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2006Article
- Anti-Fas mAb-induced apoptosis and cytolysis of airway tissue eosinophils aggravates rather than resolves established inflammation.Respiratory research · 2005Article
- Adenovirus expressing Fas ligand gene decreases airway hyper-responsiveness and eosinophilia in a murine model of asthma.Gene therapy · 2004Article
- Excretory-secretory product of newly excysted metacercariae of Paragonimus westermani directly induces eosinophil apoptosis.The Korean journal of parasitology · 2000Article
- Gene transfer into inflamed glomeruli using macrophages transfected with adenovirus.Gene therapy · 2000Article
- Disruption of fas receptor signaling by nitric oxide in eosinophils.The Journal of experimental medicine · 1998Article
- Blockade of CD49d (alpha4 integrin) on intrapulmonary but not circulating leukocytes inhibits airway inflammation and hyperresponsiveness in a mouse model of asthma.The Journal of clinical investigation · 1997Article
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
While considerable progress has been made in understanding the events by which eosinophils accumulate in various pathophysiological conditions, the mechanisms controlling the resolution of eosinophilic inflammation are poorly understood. In the present study, we demonstrate that lung eosinophils obtained by bronchoalveolar lavage (BAL) after aerosol allergen provocation of immunized mice expressed the Fas receptor. Stimulation of purified eosinophils in vitro with a monoclonal anti-Fas mAb (1 ng-1 microg/ml) induced a dose/time dependent loss of cell viability from 24-72 h. Measurement of DNA fragmentation with propidium iodide confirmed that anti-Fas induced eosinophil death by apoptosis. While incubation with IL-3, IL-5, or GM-CSF prevented spontaneous apoptosis, these factors failed to prevent anti-Fas induced apoptosis. Administration of anti-Fas mAb to the lungs after the induction of a lung eosinophilia increased the number of peroxidase positive macrophages in BAL fluid 4-12 h later which was followed by a marked reduction in the number of eosinophils in the airways. Importantly, Fas-mediated resolution of eosinophilic inflammation occurred in the absence of any overt secondary inflammatory changes in the lungs. We speculate that defects in this pathway may at least in part explain the chronic eosinophilic inflammation often observed in the lungs of asthmatic individuals.
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