It has been reported that infectious mononucleosis (IM)-symptomatic primary Epstein-Barr virus infection produces a global down-regulation of interleukin-15 receptor-α (IL-15Rα) 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-15Rα 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. © 2009 by The American Society of Hematology.
|Titolo:||EBV-associated mononucleosis does not induce long-term global deficit in T-cell responsiveness to IL-15|
|Data di pubblicazione:||2009|
|Appare nelle tipologie:||01.01 - Articolo su rivista|
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|EBV-associated mononucleosis does not induce long-term global deficit in T-cell responsiveness to IL-15..pdf||EBV-associated mononucleosis does not induce long-term global deficit in T-cell responsiveness to IL-15.||Documento in versione editoriale||Open Access Visualizza/Apri|