EBV-associated mononucleosis does not induce long-term global deficit in T-cell responsiveness to IL-15.
It has been reported that infectious mononucleosis (IM)-symptomatic primary Epstein-Barr virus infection produces a global down-regulation of interleukin-15 receptor-alpha (IL-15Ralpha) 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-15Ralpha 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.
Giron-Michel
Julien
J
Inserm Unite Mixte de Recherche 542, Université de Paris-Sud, Hôpital Paul Brousse, Villejuif, France.
Menard
Fanny
F
Negrini
Simone
S
Devocelle
Aurore
A
Azzarone
Bruno
B
Besson
Caroline
C
D017209:Apoptosis / Q000502:physiology; D015153:Blotting, Western; D018414:CD8-Positive T-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000821:virology; D016022:Case-Control Studies; D020031:Epstein-Barr Virus Infections / Q000276:immunology* / Q000821:virology; D005434:Flow Cytometry; D004854:Herpesvirus 4, Human / Q000472:pathogenicity*; D006801:Humans; D007244:Infectious Mononucleosis / Q000276:immunology* / Q000821:virology; D019409:Interleukin-15 / Q000494:pharmacology*; D053720:Interleukin-15 Receptor alpha Subunit / Q000378:metabolism; D010766:Phosphorylation; D050799:STAT5 Transcription Factor
D019409:Interleukin-15; D053720:Interleukin-15 Receptor alpha Subunit; D050799:STAT5 Transcription Factor