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 Blood, 15 February 2005, Vol. 105, No. 4, pp. 1632-1639.
Prepublished online as a Blood First Edition Paper on October 21, 2004; DOI 10.1182/blood-2004-08-3196.

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IMMUNOBIOLOGY

Epstein-Barr virus nuclear antigen 2 induces interleukin-18 receptor expression in B cells

Franck Pagès, Jérôme Galon, Galina Karaschuk, Diana Dudziak, Mathieu Camus, Vladimir Lazar, Sophie Camilleri-Broët, Christine Lagorce-Pagès, Sophie Lebel-Binay, Gerhard Laux, Wolf-Herman Fridman, and Berthold Henglein

From Institut National de la Santé et de la Recherche Médicale (INSERM) U 255, Centre de Recherches Biomédicales des Cordeliers, Paris, France; Hôpital Européen Georges Pompidou, AP-HP, Service d'Immunologie Biologique, Paris, France; GSF-Forschungszentrum für Umwelt und Gesundheit, Institut für Klinische Molekularbiologie und Tumorgenetik, München, Germany; Institut Gustave Roussy, Unité de Génomique Fonctionnelle, Villejuif, France; Hôpital Hôtel-Dieu, AP-HP, Service d'Anatomie Pathologique, Paris, France; Hôpital Avicenne, AP-HP, Service d'Anatomie Pathologique, Bobigny, France; and Centre National de la Recherche Scientifique (CNRS) Unité Mixté de Recherche (UMR) 7098, Université Pierre et Marie Curie, Paris, France

Epstein-Barr virus (EBV) latently infects and immortalizes B lymphocytes and causes lymphoproliferative malignancies. We show here that the EBV nuclear antigen EBNA2 induces expression of the 2 chains of the interleukin-18 receptor (IL-18R) in Burkitt lymphoma (BL) cell lines and in nontransformed B cells. Activation of IL-18R expression by EBNA2 is independent of its interaction with the transcriptional repressor RBPJ{kappa}. It occurs in the absence of any other viral protein but requires de novo synthesis of cellular proteins. IL-18R induction is a highly specific function of EBNA2, because neither other EBV latent proteins nor the cellular proteins c-myc or Notch can exert this effect. Using cDNA microarray expression profiling, we find that the IL-18 receptor expressed in EBV-infected BL cells has signaling capacity, because IL-18 significantly modified gene expression. We report that EBNA2 expression is associated with IL-18R expression in vivo in EBV-positive B-lymphomas from AIDS patients. (Blood. 2005;105:1632-1639)


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