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Blood, 1 April 2006, Vol. 107, No. 7, pp. 2928-2935. Prepublished online as a Blood First Edition Paper on December 6, 2005; DOI 10.1182/blood-2005-06-2569. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-06-2569v1 107/7/2928    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kis, L. L. Articles by Klein, E. Search for Related Content PubMed PubMed Citation Articles by Kis, L. L. Articles by Klein, E. Related Collections Immunobiology Neoplasia Signal Transduction Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA IL-10 can induce the expression of EBV-encoded latent membrane protein-1 (LMP-1) in the absence of EBNA-2 in B lymphocytes and in Burkitt lymphoma- and NK lymphoma-derived cell lines Lorand L. Kis, Miki Takahara, Noemi Nagy, George Klein, and Eva Klein From the Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden. EBV-positive nasopharyngeal carcinoma and Hodgkin, T, and natural killer (NK) lymphomas express EBNA-1 and the latent membrane proteins (LMP1-2; type II latency). In contrast to type III EBV-transformed lymphoblastoid cell lines, in these cells the LMPs are expressed in the absence of EBNA-2. We have previously reported that exposure to CD40 ligand and IL-4 could induce LMP-1 in an in vitro EBV-infected Hodgkin lymphoma-derived cell line, which expressed only EBNA-1. We show now that both human and EBV-encoded IL-10 can induce LMP-1 in the absence of EBNA-2 in the Daudi, P3HR1, and other BL cell lines. Interestingly, induction of LMP-1 was not accompanied by the downregulation of BCL-6. IL-10 could also induce LMP-1 in the conditional lymphoblastoid cell line ER/EB2-5 where EBNA-2 was downregulated in the absence of estrogen. Moreover, IL-10 could induce the expression of LMP-1 in tonsillar B cells infected with the nontransforming, EBNA-2-deficient EBV strain P3HR1 and enhance LMP-1 expression in 2 EBV-positive NK lymphoma lines. The demonstration that IL-10 can induce the expression of LMP-1 in an EBNA-2-independent manner shows that the major transforming EBV gene LMP-1 can be induced by extracellular signals in lymphoid cells, and IL-10 might contribute to the establishment of type II EBV latency. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Host EBV communication David A. Thorley-Lawson Blood 2006 107: 2592-2593. [Full Text] [PDF] This article has been cited by other articles: J. Garibal, E. Hollville, A. I. Bell, G. L. Kelly, B. Renouf, Y. Kawaguchi, A. B. Rickinson, and J. Wiels Truncated Form of the Epstein-Barr Virus Protein EBNA-LP Protects against Caspase-Dependent Apoptosis by Inhibiting Protein Phosphatase 2A J. Virol., July 15, 2007; 81(14): 7598 - 7607. [Abstract] [Full Text] [PDF] G. Goormachtigh, T.-S. Ouk, A. Mougel, D. Tranchand-Bunel, E. Masy, C. Le Clorennec, J. Feuillard, G. W. Bornkamm, C. Auriault, E. Manet, et al. Autoactivation of the Epstein-Barr Virus Oncogenic Protein LMP1 during Type II Latency through Opposite Roles of the NF-{kappa}B and JNK Signaling Pathways. J. Virol., August 1, 2006; 80(15): 7382 - 7393. [Abstract] [Full Text] [PDF]

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