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Blood, 7 May 2009, Vol. 113, No. 19, pp. 4541-4547. Prepublished online as a Blood First Edition Paper on March 4, 2009; DOI 10.1182/blood-2008-12-195289. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2008-12-195289v1 113/19/4541    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Giron-Michel, J. Articles by Besson, C. Search for Related Content PubMed PubMed Citation Articles by Giron-Michel, J. Articles by Besson, C. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY EBV-associated mononucleosis does not induce long-term global deficit in T-cell responsiveness to IL-15 Julien Giron-Michel1,*, Fanny Menard2,3,*, Simone Negrini1,4, Aurore Devocelle1, Bruno Azzarone1,*, and Caroline Besson2,3,* 1 Inserm Unite Mixte de Recherche 542, Université de Paris-Sud, Hôpital Paul Brousse, Villejuif, France; 2 Inserm U802, Université de Paris-Sud, Paris, France; 3 Service d'Hématologie et Immunologie Biologiques, Cytogénétique, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris, Le Kremlin-Bicêtre, Paris, France; and 4 Department of Internal Medicine, University of Genoa, Genoa, Italy It has been reported that infectious mononucleosis (IM)–symptomatic primary Epstein-Barr virus infection produces a global down-regulation of interleukin-15 receptor- (IL-15R) on T cells and natural killer cells associated with a defective IL-15 responsiveness that lasts for many years after the disease episode. In contrast with these results, our data indicate that, in the T-cell compartment derived from remote IM subjects, there is no quantitative or qualitative defect in the expression of the IL-15R chain and no deficit in T-cell responsiveness to IL-15. We observed efficient signal transduction, survival, and proliferation even in response to low IL-15 concentrations. These data are relevant and shed new light on the immune long-term response in IM subjects because they contradict the hypothesis that defects in Epstein-Barr virus–host immune balance may be correlated with a long-lasting global deficit in T-cell responsiveness to IL-15. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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