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Anti-Fas/CD95 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) differentially regulate apoptosis in normal and neoplastic human basophils

Förster, Anja and Falcone, Franco H. and Gibbs, Bernhard F. and Preussner, Liane M. and Fiebig, Britta S. and Altunok, Hülya and Seeger, Jens M. and Cerny-Reiterer, Sabine and Rabenhorst, Anja and Papenfuss, Kerstin and Valent, Peter and Kashkar, Hamid and Hartmann, Karin. (2013) Anti-Fas/CD95 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) differentially regulate apoptosis in normal and neoplastic human basophils. Leukemia & lymphoma, 54 (4). pp. 835-842.

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Official URL: https://edoc.unibas.ch/70803/

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Abstract

Basophilia is associated with allergic and parasitic diseases and advanced chronic myeloid leukemia. In the present study, we characterized the expression and function of the death receptors Fas/CD95 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors in basophils from healthy donors compared to neoplastic basophils. Peripheral blood basophils obtained from healthy donors (HD-PBB) and from patients with chronic myeloid leukemia (CML-PBB) were found to express high levels of Fas/CD95 and low levels of TRAIL-R2, whereas the basophil-like chronic myeloid leukemia cell line KU-812 expressed significant levels of TRAIL-R1 and TRAIL-R2. HD-PBB underwent apoptosis in response to anti-Fas/CD95, but showed resistance to TRAIL, unless they were co-treated with actinomycin D. Interestingly, CML-PBB and KU-812 cells exhibited the opposite response pattern with resistance to anti-Fas/CD95, but significant susceptibility to TRAIL-induced apoptosis. Our data show that anti-Fas/CD95 and TRAIL differentially regulate apoptosis of normal and neoplastic human basophils, which may direct the development of novel therapeutic strategies.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Allergy and Immunity (Hartmann)
UniBasel Contributors:Hartmann, Karin
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Taylor & Francis
ISSN:1042-8194
e-ISSN:1029-2403
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:10 Nov 2020 17:01
Deposited On:10 Nov 2020 17:01

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