Epstein-Barr Virus Nuclear Antigen Leader Protein Induces Expression of Thymus- and Activation-Regulated Chemokine in B Cells

  • Mikiko Kanamori
    Department of Virology, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550
  • Shinya Watanabe
    Division of Cancer Genomics, Department of Cancer Biology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639
  • Reiko Honma
    Division of Cancer Genomics, Department of Cancer Biology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639
  • Masayuki Kuroda
    Department of Molecular Microbiology and Infections Program of Bio-signaling and Infection Control, Kochi Medical School, Kochi 783-8505
  • Shosuke Imai
    Department of Molecular Microbiology and Infections Program of Bio-signaling and Infection Control, Kochi Medical School, Kochi 783-8505
  • Kenzo Takada
    Department of Tumor Virology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan
  • Naoki Yamamoto
    Department of Molecular Virology, Tokyo Medical and Dental University School of Medicine, Bunkyo-ku, Tokyo 113-8519
  • Yukihiro Nishiyama
    Department of Virology, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550
  • Yasushi Kawaguchi
    Department of Virology, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550

抄録

<jats:title>ABSTRACT</jats:title><jats:p>Epstein-Barr virus (EBV) nuclear antigen leader protein (EBNA-LP) plays a critical role in transformation of primary B lymphocytes to continuously proliferating lymphoblastoid cell lines (LCLs). To identify cellular genes in B cells whose expression is regulated by EBNA-LP, we performed microarray expression profiling on an EBV-negative human B-cell line, BJAB cells, that were transduced by a retroviral vector expressing the EBV EBNA-LP (BJAB-LP cells) and on BJAB cells that were transduced with a control vector (BJAB-vec cells). Microarray analysis led to the identification of a cellular gene encoding the CC chemokine TARC as a novel target gene that was induced by EBNA-LP. The levels of TARC mRNA expression and TARC secretion were significantly up-regulated in BJAB-LP compared with BJAB-vec cells. Induction of TARC was also observed when a subline of BJAB cells was converted by a recombinant EBV. Among the EBV-infected B-cell lines with the latency III phenotype that were tested, the LCLs especially secreted significantly high levels of TARC. The level of TARC secretion appeared to correlate with the level of full-length EBNA-LP expression. These results indicate that EBV infection induces TARC expression in B cells and that EBNA-LP is one of the viral gene products responsible for the induction.</jats:p>

収録刊行物

  • Journal of Virology

    Journal of Virology 78 (8), 3984-3993, 2004-04-15

    American Society for Microbiology

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