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Blood, 15 December 2005, Vol. 106, No. 13, pp. 4345-4350. Prepublished online as a Blood First Edition Paper on August 30, 2005; DOI 10.1182/blood-2005-06-2342. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-06-2342v1 106/13/4345    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 Bechtel, D. Articles by Küppers, R. Search for Related Content PubMed PubMed Citation Articles by Bechtel, D. Articles by Küppers, R. Related Collections Immunobiology Neoplasia Related Articles in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Transformation of BCR-deficient germinal-center B cells by EBV supports a major role of the virus in the pathogenesis of Hodgkin and posttransplantation lymphomas Dörte Bechtel, Julia Kurth, Claus Unkel, and Ralf Küppers From the Institute for Cell Biology (Tumor Research), University of Duisburg-Essen, Essen, Germany; and the Department of Otorhinolaryngology, University of Duisburg-Essen, Essen, Germany. In classic Hodgkin lymphoma (HL) and posttransplantation lymphoproliferative disease (PTLD), 2 malignancies frequently associated with Epstein-Barr virus (EBV), the tumor cells often appear to derive from B-cell receptor (BCR)–deficient and therefore preapoptotic germinal center (GC) B cells. To test whether EBV can rescue BCR-less GC B cells, we infected human tonsillar CD77+ GC B cells in vitro with EBV. More than 60 monoclonal lymphoblastoid cell lines (LCLs) were established. Among these, 28 cell lines did not express surface immunoglobulin (sIg). Two of the sIg-negative cell lines carry obviously destructive mutations that have been introduced into originally functional VH gene rearrangements during the process of somatic hypermutation. Quantitative reverse transcriptase–polymerase chain reaction (RT-PCR) showed that in most other lines the sIg deficiency was not simply the result of transcriptional down-regulation, but it was rather due to posttranscriptional defects. These findings strongly support the idea that EBV plays a central role in the pathogenesis of classic HL and PTLD by rescuing BCR-deficient, preapoptotic GC B cells from apoptosis, and that EBV infection renders the cells independent from survival signals normally supplied by a BCR. The monoclonal LCLs represent valuable models for early stages of lymphoma development in classic HL and PTLD. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Articles in Blood Online: EBV meets BCR- B cells Daniel Re Blood 2005 106: 4020-4021. [Full Text] [PDF] Rescue of "crippled" germinal center B cells from apoptosis by Epstein-Barr virus Christoph Mancao, Markus Altmann, Berit Jungnickel, and Wolfgang Hammerschmidt Blood 2005 106: 4339-4344. [Abstract] [Full Text] [PDF] This article has been cited by other articles: R. M'kacher, L. Andreoletti, S. Flamant, F. Milliat, T. Girinsky, J. Dossou, D. Violot, E. Assaf, B. Clausse, S. Koscielny, et al. JC human polyomavirus is associated to chromosomal instability in peripheral blood lymphocytes of Hodgkin's lymphoma patients and poor clinical outcome Ann. Onc., October 13, 2009; (2009) mdp375v1. [Abstract] [Full Text] [PDF] G Kapatai and P Murray Contribution of the Epstein Barr virus to the molecular pathogenesis of Hodgkin lymphoma J. Clin. Pathol., December 1, 2007; 60(12): 1342 - 1349. [Abstract] [Full Text] [PDF] R. Kuppers Viral mimic for B-cell survival Blood, November 15, 2007; 110(10): 3494 - 3495. [Full Text] [PDF] C. Mancao and W. Hammerschmidt Epstein-Barr virus latent membrane protein 2A is a B-cell receptor mimic and essential for B-cell survival Blood, November 15, 2007; 110(10): 3715 - 3721. [Abstract] [Full Text] [PDF] R. F. Ambinder Epstein-Barr Virus and Hodgkin Lymphoma Hematology, January 1, 2007; 2007(1): 204 - 209. [Abstract] [Full Text] [PDF] Y. Natkunam The Biology of the Germinal Center Hematology, January 1, 2007; 2007(1): 210 - 215. [Abstract] [Full Text] [PDF] Y. Natkunam, E. D. Hsi, P. Aoun, S. Zhao, P. Elson, B. Pohlman, H. Naushad, M. Bast, R. Levy, and I. S. Lossos Expression of the human germinal center-associated lymphoma (HGAL) protein identifies a subset of classic Hodgkin lymphoma of germinal center derivation and improved survival Blood, January 1, 2007; 109(1): 298 - 305. [Abstract] [Full Text] [PDF] S. Tobollik, L. Meyer, M. Buettner, S. Klemmer, B. Kempkes, E. Kremmer, G. Niedobitek, and B. Jungnickel Epstein-Barr virus nuclear antigen 2 inhibits AID expression during EBV-driven B-cell growth Blood, December 1, 2006; 108(12): 3859 - 3864. [Abstract] [Full Text] [PDF] A. L. Snow, S. L. Lambert, Y. Natkunam, C. O. Esquivel, S. M. Krams, and O. M. Martinez EBV Can Protect Latently Infected B Cell Lymphomas from Death Receptor-Induced Apoptosis. J. Immunol., September 1, 2006; 177(5): 3283 - 3293. [Abstract] [Full Text] [PDF] S. Chaganti, A. I. Bell, N. B. Pastor, A. E. Milner, M. Drayson, J. Gordon, and A. B. Rickinson Epstein-Barr virus infection in vitro can rescue germinal center B cells with inactivated immunoglobulin genes Blood, December 15, 2005; 106(13): 4249 - 4252. [Abstract] [Full Text] [PDF] C. Mancao, M. Altmann, B. Jungnickel, and W. Hammerschmidt Rescue of "crippled" germinal center B cells from apoptosis by Epstein-Barr virus Blood, December 15, 2005; 106(13): 4339 - 4344. [Abstract] [Full Text] [PDF]

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