CD80 (B7.1) and CD86 (B7.2) induce EBV-transformed B cell apoptosis through the Fas/FasL pathway

Ga Bin Park, Yeong Seok Kim, Hyun Kyung Lee, Dae Ho Cho, Daejin Kim, Dae Young Hur

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


CD80 and CD86 expression is strongly regulated in B cells and is induced by various stimuli (e.g., cytokines, ligation of MHC class II and CD40 ligand). Epstein-Barr virus (EBV) infection activates B lymphocytes and transforms them into lymphoblastoid cells. However, the role of CD80 and CD86 in EBV infection of B cells remains unclear. Here, we observed that cross-linking of CD80 and CD86 in EBV-transformed B cells induced apoptosis through caspase-dependent release of apoptosis-related molecules, cytochrome c and apoptosis-inducing factor (AIF) from mitochondria, because Z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala- Asp-fluoromethylketone) and N-acetylcysteine (NAC) blocked apoptosis and disruption of mitochondria. Stimulation of CD80 and CD86 induced expression of Fas ligand (FasL) on EBV-transformed B cells and upregulated Fas and FasL expression in IM-9 cells. Apoptosis through Fas-FasL interactions was blocked by treatment of cells with ZB4, an antagonistic anti-Fas antibody. These results suggest that the co-stimulatory molecules CD80 and CD86 induced by EBV infection stimulate apoptosis of EBV-transformed lymphoblastoid B cells via the Fas/FasL pathway.

Original languageEnglish
Pages (from-to)1531-1540
Number of pages10
JournalInternational journal of oncology
Issue number5
Publication statusPublished - 2013 Nov
Externally publishedYes


  • Apoptosis
  • B cells
  • CD80
  • CD86
  • Epstein-Barr virus

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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