Critical role for mitochondria in B cell receptor-mediated apoptosis

• Verfasst von: Bouchon, Axel [VerfasserIn]
• Verfasst von: Krammer, Peter H. [VerfasserIn]
• Verfasst von: Walczak, Henning [VerfasserIn]
• Titel: Critical role for mitochondria in B cell receptor-mediated apoptosis
• Verf.angabe: Axel Bouchon, Peter H. Krammer and Henning Walczak
• E-Jahr: 2000
• Jahr: 30 August 2000
• Umfang: 9 S.
• Teil: volume:30
• Teil: year:2000
• Teil: number:1
• Teil: pages:69-77
• Teil: extent:9
• Fussnoten: Gesehen am 26.04.2021 ; DOI funktioniert nicht
• Titel Quelle: Enthalten in: European journal of immunology
• Ort Quelle: Weinheim : Wiley-VCH, 1971
• Jahr Quelle: 2000
• Band/Heft Quelle: 30(2000), 1, Seite 69-77
• ISSN Quelle: 1521-4141
• DOI: doi:10.1002/1521-4141(200001)30:1<69::AID-IMMU69>3.0.CO;2-#
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Activation-induced cell death
• Sach-SW: B cell
• Sach-SW: Caspase
• Sach-SW: Death receptor
• Sach-SW: Mitochondrial permeability transition
• K10plus-PPN: 1755910010

Abstract

Antigen-induced apoptosis of B cells serves to deplete the immune repertoire of anti-self specificities leading to central and peripheral B cell tolerance. However, the mechanism of B cell receptor (BCR)-mediated apoptosis is widely unknown. By using the human Burkitt lymphoma cell line BL60 as a model system for human germinal center B cells we show here that BCR-mediated apoptosis requires transcriptional activity but, in contrast to activation-induced T cell apoptosis, is neither mediated via known death receptor systems nor does it involve initial activation of caspase-8. Moreover, during BCR-induced apoptosis cytochrome c release and mitochondrial permeability transition (PT) precedecaspase activation. Although caspase inhibition after BCR stimulation blocks cleavage of caspase substrates and DNA fragmentation it does not prevent mitochondrial PT, cytochrome c release and cell death. Thus, BCR-mediated apoptosis is initiated by the caspase-independent induction of mitochondrial PT resulting in release of cytochrome c and subsequent activation of caspase-9, downstream caspases and apoptosis.