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

Abstract

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.

• Authors: Julien Giron-Michel, Fanny Menard, Simone Negrini, Aurore Devocelle, Bruno Azzarone, Caroline Besson
• Journal: Blood (Blood) Vol. 113 Issue 19 Pg. 4541-7 (May 07 2009) ISSN: 1528-0020 [Electronic] United States
• PMID: 19264676 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Interleukin-15
• Interleukin-15 Receptor alpha Subunit
• STAT5 Transcription Factor

Topics

• Apoptosis (physiology)
• Blotting, Western
• CD8-Positive T-Lymphocytes (cytology, immunology, virology)
• Case-Control Studies
• Epstein-Barr Virus Infections (immunology, virology)
• Flow Cytometry
• Herpesvirus 4, Human (pathogenicity)
• Humans
• Infectious Mononucleosis (immunology, virology)
• Interleukin-15 (pharmacology)
• Interleukin-15 Receptor alpha Subunit (metabolism)
• Phosphorylation
• STAT5 Transcription Factor