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Cancer Lett. 2008 Aug 8;266(2):227-37. doi: 10.1016/j.canlet.2008.02.067. Epub 2008 Apr 15.

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

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Department of Anatomy and Tumor Immunology, Inje University College of Medicine, 633-165 Kaekum-2-dong, Jin-gu, Busan 614-735, Republic of Korea.


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 c 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.

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