title: Transient expression of the Epstein-Barr virus LMP1 gene in B-cell chronic lymphocytic leukemia cells, T cells, and hematopoietic cell lines: cell-type-independent-induction of CD23, CD21, and ICAM-1.
abstract: The Epstein-Barr virus (EBV) genome has recently been detected in various non-B cell neoplasms, including various T-cell leukemias and in Reed-Sternberg cells of Hodgkin's disease, but the contribution of EBV genes to the transformed phenotype remains unclear. We have investigated the possible effect which the EBV genes LMP1 and EBNA2, of which the expression has been reported in non-B cell neoplasms, may have on a variety of cell types. The LMP1 and EBNA2 genes were transiently expressed from heterologous promoters in two human T-cell lines (HPB-ALL and Jurkat), two human cell lines of the myeloid lineage (K562 and U937), one type I Burkitt's lymphoma cell line (Rael) and in human primary T cells and B-cell chronic lymphocytic leukemia cells. The cell surface expression of CD23, CD21, ICAM-1 and LFA-1 was monitored on transfected cells. In the cell lines, except U937, the surface antigens CD21 and ICAM-1 were upregulated in a dose-dependent and transient manner by the transient expression of LMP1, and EBNA2 slightly enhanced the effects of LMP1 on CD23 and CD21 upregulation. LMP1 also induced increased CD21, ICAM-1 and LFA-1 surface expression on transfected primary T-cells, and CD21 and ICAM-1 in four of five B-cell chronic lymphocytic leukemias tested. Finally, LMP1 transient expression caused increased cell size of the primary T cells and responding B-cell chronic lymphocytic leukemia cells. Our results strongly suggest that LMP1 can trigger specific responses in a variety of white cell types and thus is probably contributing to the phenotype of EBV-positive tumor cells not only in the B-cell lineage.
authors.affiliation: Unit for Applied Cell and Molecular Biology, University of Umeå, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Peng
authors.forename: E
authors.initials: E
authors.lastname: Lundgren
mesh_terms: D000956:Antigens, Viral / Q000235:genetics* / Q000378:metabolism; D002213:Capsid / Q000235:genetics / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000096:biosynthesis*; D048429:Cell Size; D004268:DNA-Binding Proteins / Q000235:genetics; D019309:Epstein-Barr Virus Nuclear Antigens; D015870:Gene Expression; D005814:Genes, Viral; D006412:Hematopoietic Stem Cells / Q000382:microbiology*; D004854:Herpesvirus 4, Human / Q000235:genetics*; D006801:Humans; D066298:In Vitro Techniques; D018799:Intercellular Adhesion Molecule-1; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000382:microbiology*; D008565:Membrane Proteins / Q000235:genetics* / Q000378:metabolism; D017464:Receptors, Complement 3d / Q000096:biosynthesis*; D017455:Receptors, IgE / Q000096:biosynthesis*; D013601:T-Lymphocytes / Q000382:microbiology*; D014407:Tumor Cells, Cultured; D014763:Viral Matrix Proteins; D015678:Viral Structural Proteins / Q000235:genetics
chemical_list: D000956:Antigens, Viral; D015815:Cell Adhesion Molecules; D004268:DNA-Binding Proteins; C037662:EBV-associated membrane antigen, Epstein-Barr virus; D019309:Epstein-Barr Virus Nuclear Antigens; D008565:Membrane Proteins; D017464:Receptors, Complement 3d; D017455:Receptors, IgE; D014763:Viral Matrix Proteins; D015678:Viral Structural Proteins; D018799:Intercellular Adhesion Molecule-1