B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation
- Authors
- Song, Hyunkeun; Park, Gabin; Kim, Yeong-Seok; Hur, Indo; Kim, Hyunjin; Ryu, Jeoung Whan; Lee, Hyun-Kyung; Cho, Dae-Ho; Choi, In-Hak; Lee, Wang Jae; Hur, 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.
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