title: Epstein-Barr virus (EBV)-containing nasopharyngeal carcinoma cells express the B-cell activation antigen blast2/CD23 and low levels of the EBV receptor CR2.
abstract: Anaplastic nasopharyngeal carcinoma (NPC) cells invariably harbor the Epstein-Barr virus (EBV) genome, an association that is unique among human virus-associated cancers. Although EBV is able to replicate in epithelial cells, results with expression of the EBV receptor (complement receptor type 2 [CR2]; also called CD21) in normal and malignant epithelial cells are conflicting. We grew five different EBV-associated NPC tumors in nude mice, and by using a sensitive transcriptional assay, we detected a very weak transcription signal of the EBV receptor CR2 gene in these cells. This suggests that low levels of EBV receptor may be expressed by malignant epithelial nasopharyngeal cells. The gene coding for Blast2/CD23, a B-cell activation molecule induced by EBV, was transcribed in three of the transplanted NPC tumors. The soluble form of the Blast2/CD23 protein was also detected in medium taken from short-term cultures of the same NPC cell lines. In contrast to the lymphoid system, in which Blast2/CD23 expression is associated with EBV nuclear antigen (EBNA2) expression, no EBNA2 protein could be detected in these NPC epithelial cells. Our study represents the first demonstration of Blast2/CD23 expression in epithelial cells. As the soluble form of the Blast2/CD23 protein possesses growth factor activity associated with EBV-induced B-cell immortalization, these results suggest a possible role for this molecule in the pathogenesis of NPC.
authors.affiliation: International Agency for Research on Cancer, Lyon, France.
authors.forename: M
authors.initials: M
authors.lastname: Billaud
authors.forename: P
authors.initials: P
authors.lastname: Busson
authors.forename: D
authors.initials: D
authors.lastname: Huang
authors.forename: N
authors.initials: N
authors.lastname: Mueller-Lantzch
authors.forename: G
authors.initials: G
authors.lastname: Rousselet
authors.forename: O
authors.initials: O
authors.lastname: Pavlish
authors.forename: H
authors.initials: H
authors.lastname: Wakasugi
authors.forename: J M
authors.initials: JM
authors.lastname: Seigneurin
authors.forename: T
authors.initials: T
authors.lastname: Tursz
authors.forename: G M
authors.initials: GM
authors.lastname: Lenoir
mesh_terms: D000818:Animals; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis* / Q000235:genetics; D000956:Antigens, Viral / Q000032:analysis / Q000235:genetics; D002277:Carcinoma / Q000276:immunology*; D019309:Epstein-Barr Virus Nuclear Antigens; D004854:Herpesvirus 4, Human / Q000235:genetics; D006801:Humans; D051379:Mice; D009303:Nasopharyngeal Neoplasms / Q000276:immunology*; D009368:Neoplasm Transplantation; D012333:RNA, Messenger / Q000032:analysis; D011951:Receptors, Complement / Q000032:analysis* / Q000235:genetics; D017464:Receptors, Complement 3d; D011961:Receptors, Fc / Q000032:analysis* / Q000235:genetics; D017455:Receptors, IgE; D014158:Transcription, Genetic; D014183:Transplantation, Heterologous
chemical_list: D000944:Antigens, Differentiation, B-Lymphocyte; D000956:Antigens, Viral; D019309:Epstein-Barr Virus Nuclear Antigens; D012333:RNA, Messenger; D011951:Receptors, Complement; D017464:Receptors, Complement 3d; D011961:Receptors, Fc; D017455:Receptors, IgE