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Verfasst von:Shinbori, Toshifumi [VerfasserIn]   i
 Walczak, Henning [VerfasserIn]   i
 Krammer, Peter H. [VerfasserIn]   i
Titel:Activated T killer cells induce apoptosis in lung epithelial cells and the release of pro-inflammatory cytokine TNF-α
Verf.angabe:Toshifumi Shinbori, Henning Walczak, Peter H. Krammer
E-Jahr:2004
Jahr:18 May 2004
Umfang:9 S.
Teil:volume:34
 year:2004
 number:6
 pages:1762-1770
 extent:9
Fussnoten:Gesehen am 04.03.2021
Titel Quelle:Enthalten in: European journal of immunology
Ort Quelle:Weinheim : Wiley-VCH, 1971
Jahr Quelle:2004
Band/Heft Quelle:34(2004), 6, Seite 1762-1770
ISSN Quelle:1521-4141
Abstract:Apoptosis is thought to be involved in lung epithelial cell damage in acute respiratory distress syndrome and interstitial pneumonia. Both the role of apoptosis and its underlying molecular mechanisms in human lung tissue remain unclear. To address these issues, we developed an in vitro assay in which a human lung epithelial cell line and a staphylococcal enterotoxin B (SEB)-reactive human CD8+ CTL line were co-cultured in the presence of SEB. SEB-stimulated CD8+ CTL induced apoptosis in the lung epithelial cell line primarily through the perforin/granzyme-mediated pathway. In these cells, apoptosis was initially independent of death receptor pathways. We also tested the effect of IFN-γ on modulation of apoptosis in lung epithelial cells. In IFN-γ-pretreated lung epithelial cells, CD95 (APO-1/Fas) activation as well as TNF-related apoptosis-inducing ligand (TRAIL) receptor and TNFR activation led to apoptosis. Furthermore, we found that the interaction of SEB-stimulated CD8+ CTL with lung epithelial cells induced an increase in TNF-α secretion. These results suggest an important role for bacterial superantigen-reactive CD8+ CTL in induction of lung epithelial cell apoptosis and in modulation of inflammatory processes in lung tissue.
DOI:doi:10.1002/eji.200425097
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1002/eji.200425097
 Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1002/eji.200425097
 DOI: https://doi.org/10.1002/eji.200425097
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Apoptosis
 CTL
 Interstitial pneumonia
 Pro-inflammatory cytokine
K10plus-PPN:1750439867
Verknüpfungen:→ Zeitschrift

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