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Bcl-2-mediated regulation of CD69-induced apoptosis of human eosinophils: identification and characterization of a novel receptor-induced mechanism and relationship to CD95-transduced signalling.
Scand J Immunol. 2002 Oct; 56(4):417-28.SJ

Abstract

Elimination of the eosinophils from the airways by selective induction of apoptosis represents a therapeutic approach for asthma. Here we report on a possible target molecule, the surface receptor CD69. To simulate an asthmatic response, segmental allergen challenge in mild asthmatics was performed. Eosinophil numbers increased in bronchoalveolar lavage (BAL) at 18 h. In contrast to blood cells, BAL eosinophils expressed the activation marker CD69. Purified blood eosinophils stimulated with granulocyte/macrophage colony-stimulating factor (GM-CSF) or interferon-gamma (IFN-gamma) expressed CD69 and showed prolonged viability. Only IFN-gamma enhanced constitutive CD95 expression. Coincubation with anti-CD69 or anti-CD95 monoclonal antibody (MoAb) induced apoptosis, as revealed by propidium iodide incorporation, membrane blebbing and nuclear fragmentation. Additionally, both anti-CD69 and anti-CD95 MoAb reduced cytokine-enhanced Bcl-2 expression. In conclusion, CD69 transduces a Bcl-2-dependent death signal when ligated by a specific antibody. As, in contrast to the ubiquitous death-inducer CD95, the function of CD69 appears to be restricted to activated eosinophils, it represents an ideal target for therapeutic intervention in asthma.

Authors+Show Affiliations

Pneumology, Medical Clinic IV, Friedrich-Schiller University, Jena, Germany. martin.foerster@med.uni-jena.deNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12234263

Citation

Foerster, M, et al. "Bcl-2-mediated Regulation of CD69-induced Apoptosis of Human Eosinophils: Identification and Characterization of a Novel Receptor-induced Mechanism and Relationship to CD95-transduced Signalling." Scandinavian Journal of Immunology, vol. 56, no. 4, 2002, pp. 417-28.
Foerster M, Haefner D, Kroegel C. Bcl-2-mediated regulation of CD69-induced apoptosis of human eosinophils: identification and characterization of a novel receptor-induced mechanism and relationship to CD95-transduced signalling. Scand J Immunol. 2002;56(4):417-28.
Foerster, M., Haefner, D., & Kroegel, C. (2002). Bcl-2-mediated regulation of CD69-induced apoptosis of human eosinophils: identification and characterization of a novel receptor-induced mechanism and relationship to CD95-transduced signalling. Scandinavian Journal of Immunology, 56(4), 417-28.
Foerster M, Haefner D, Kroegel C. Bcl-2-mediated Regulation of CD69-induced Apoptosis of Human Eosinophils: Identification and Characterization of a Novel Receptor-induced Mechanism and Relationship to CD95-transduced Signalling. Scand J Immunol. 2002;56(4):417-28. PubMed PMID: 12234263.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Bcl-2-mediated regulation of CD69-induced apoptosis of human eosinophils: identification and characterization of a novel receptor-induced mechanism and relationship to CD95-transduced signalling. AU - Foerster,M, AU - Haefner,D, AU - Kroegel,C, PY - 2002/9/18/pubmed PY - 2002/11/26/medline PY - 2002/9/18/entrez SP - 417 EP - 28 JF - Scandinavian journal of immunology JO - Scand J Immunol VL - 56 IS - 4 N2 - Elimination of the eosinophils from the airways by selective induction of apoptosis represents a therapeutic approach for asthma. Here we report on a possible target molecule, the surface receptor CD69. To simulate an asthmatic response, segmental allergen challenge in mild asthmatics was performed. Eosinophil numbers increased in bronchoalveolar lavage (BAL) at 18 h. In contrast to blood cells, BAL eosinophils expressed the activation marker CD69. Purified blood eosinophils stimulated with granulocyte/macrophage colony-stimulating factor (GM-CSF) or interferon-gamma (IFN-gamma) expressed CD69 and showed prolonged viability. Only IFN-gamma enhanced constitutive CD95 expression. Coincubation with anti-CD69 or anti-CD95 monoclonal antibody (MoAb) induced apoptosis, as revealed by propidium iodide incorporation, membrane blebbing and nuclear fragmentation. Additionally, both anti-CD69 and anti-CD95 MoAb reduced cytokine-enhanced Bcl-2 expression. In conclusion, CD69 transduces a Bcl-2-dependent death signal when ligated by a specific antibody. As, in contrast to the ubiquitous death-inducer CD95, the function of CD69 appears to be restricted to activated eosinophils, it represents an ideal target for therapeutic intervention in asthma. SN - 0300-9475 UR - https://www.unboundmedicine.com/medline/citation/12234263/Bcl_2_mediated_regulation_of_CD69_induced_apoptosis_of_human_eosinophils:_identification_and_characterization_of_a_novel_receptor_induced_mechanism_and_relationship_to_CD95_transduced_signalling_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0300-9475&date=2002&volume=56&issue=4&spage=417 DB - PRIME DP - Unbound Medicine ER -