Open AccessEnhanced susceptibility of B lymphoma cells to measles virus by E pstein– B arr virus type III latency that upregulates CD 150/signaling lymphocytic activation molecule
Author(s) -
Takeda Satoshi,
Kanbayashi Daiki,
Kurata Takako,
Yoshiyama Hironori,
Komano Jun
Publication year - 2014
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12324
Subject(s) - measles virus , cytolysis , lymphoma , virology , cell culture , b cell , oncolytic virus , epstein–barr virus , virotherapy , virus , immunology , biology , cancer research , measles , antibody , in vitro , cytotoxic t cell , vaccination , biochemistry , genetics
Measles virus ( MV ) is one of the candidates for the application of oncolytic virotherapy ( OVT ). Although an advanced clinical study has been reported on a T‐cell lymphoma, the potential of MV OVT against B‐cell lymphomas remains to be clarified. We found that an EBV ‐transformed B lymphoblastoid cell line, a model for diffuse large B‐cell lymphoma, and EBV ‐positive Burkitt's lymphoma cells bearing type III latency were highly susceptible to the cytolysis induced by an MV vaccine strain CAM ‐70. As analyzed by EBV ‐positive and ‐negative counterparts of the same cytogenetic background, type III EBV latency, not type I, was shown to augment the susceptibility of B lymphoma cells to MV ‐induced cytolysis. Cell surface levels of CD 150/signaling lymphocytic activation molecule, a receptor of MV , were upregulated in B lymphoma cell lines with type III EBV latency by 3.8‐fold, on average. The cytolytic activity of CD 150‐tropic WT MV was akin to that of CD 46‐ and CD 150‐tropic CAM ‐70, suggesting that CD 150 is critical for the susceptibility to MV ‐induced cytolysis. Among EBV ‐encoded genes, latent membrane protein 1 was responsible for the CD 150 upregulation. It was notable that the majority of B lymphoma cell lines of type III EBV latency showed higher susceptibility to the non‐Edmonston‐derived CAM ‐70 than to the Edmonston‐derived Schwarz strain. This is the first report indicating the potential of non‐Edmonston MV strain for the application of OVT . Furthermore, a cellular regulator of MV replication was implicated that functions in a vaccine strain‐specific fashion. Altogether, the MV OVT should serve as an alternative therapy against EBV ‐positive diffuse large B‐cell lymphoma with type III EBV latency.