Detailed Information

Cited 0 time in webofscience Cited 30 time in scopus
Metadata Downloads

B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation

Authors
Song, HyunkeunPark, GabinKim, Yeong-SeokHur, IndoKim, HyunjinRyu, Jeoung WhanLee, Hyun-KyungCho, Dae-HoChoi, In-HakLee, Wang JaeHur, Dae Young
Issue Date
8-Aug-2008
Publisher
ELSEVIER IRELAND LTD
Keywords
EBV; B cell; B7-H4; Fas; FasL; apoptosis
Citation
CANCER LETTERS, v.266, no.2, pp 227 - 237
Pages
11
Journal Title
CANCER LETTERS
Volume
266
Number
2
Start Page
227
End Page
237
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/14209
DOI
10.1016/j.canlet.2008.02.067
ISSN
0304-3835
1872-7980
Abstract
B7-H4 has an inhibitory effect on immune responses via the down-regulation of T cell-mediated immunity, but how the engagement of B7-H4 molecules by counter molecules affects the signaling mechanism of the B7-H4-expressing cells is poorly defined. In this study, we found that B7-H4 expression was enhanced on B cells infected with Epstein-Barr virus (EBV) and that triggering of these molecules induced apoptosis of EBV-transformed B cells. Engagement of B7-H4 initially increased intracellular level of ROS, which then induced the expression of FasL. Engagement of B7-H4 subsequently provoked Fas-mediated and caspase-dependent apoptosis in association with cytochrome e and AIF, and EndoG was released from the mitochondria on EBV-transformed B cells. These results suggest that B7-H4 may be a potential therapeutic target for EBV involved malignancy diseases. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
Files in This Item
There are no files associated with this item.
Appears in
Collections
대학 > 기초교양대학 > 기초교양학부 > 1. Journal Articles

qrcode

Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.

Altmetrics

Total Views & Downloads

BROWSE