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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.


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Submitted December 29, 2008
Accepted February 19, 2009

EBV-associated mononucleosis does not induce long-term global deficit in T-cell responsiveness to IL-15

Julien Giron-Michel, Fanny Menard, Simone Negrini, Aurore Devocelle, Bruno Azzarone*, and Caroline Besson

INSERM UMR 542, Universite de Paris-Sud, Hopital Paul Brousse, Villejuif, France
INSERM U802, Universite de Paris-Sud, F-94270, France
Department of Internal Medicine, University of Genoa, Viale Benedetto XV, Genoa, Italy
Service d'Hematologie et Immunologie Biologiques, Cytogenetique F-94270, Hopital Bicetre, Assistance Publique--Hopitaux de Paris, Le Kremlin-Bicetre, France

* Corresponding author; email: bazzarone{at}hotmail.com.

It has been reported that infectious mononucleosis (IM)- symptomatic primary Epstein-Barr virus (EBV) infection produces a global down-regulation of IL-15R{alpha} on T cells and NK cells associated to 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{alpha} 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 a new light on the immune long-term response in IM subjects since they infirm the hypothesis that defects in EBV-host immune balance may be correlated with a long-lasting global deficit in T-cell responsiveness to IL-15.


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