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Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis
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EBV-associated mononucleosis does not induce long-term global deficit in T-cell responsiveness to IL-15

Julien Giron-Michel1, Fanny Menard, Simone Negrini

  • 1Inserm Unite Mixte de Recherche 542, Université de Paris-Sud, Hôpital Paul Brousse, Villejuif, France.

Blood
|March 7, 2009
PubMed

Insights

Infectious mononucleosis (IM) does not cause long-term T-cell defects in interleukin-15 receptor-alpha (IL-15Ralpha) expression or responsiveness. This finding challenges previous hypotheses about Epstein-Barr virus-induced immune imbalances.

Area of Science:

  • Immunology
  • Virology
  • Cellular Biology

Background:

  • Infectious mononucleosis (IM), caused by Epstein-Barr virus (EBV), has been linked to long-term immune system deficits.
  • Previous studies suggested a persistent down-regulation of interleukin-15 receptor-alpha (IL-15Ralpha) on immune cells, impairing IL-15 responsiveness after IM.

Purpose of the Study:

  • To investigate the long-term effects of remote IM on T-cell expression and function of IL-15Ralpha.
  • To re-evaluate the hypothesis that EBV infection causes a lasting global deficit in T-cell responsiveness to IL-15.

Main Methods:

  • Analysis of T-cell populations from individuals with a history of remote IM.
  • Quantitative and qualitative assessment of IL-15Ralpha chain expression on T cells.
  • Evaluation of T-cell signal transduction, survival, and proliferation in response to IL-15 stimulation.

Main Results:

  • No quantitative or qualitative defect in IL-15Ralpha expression was found on T cells from remote IM subjects.
  • T cells from these individuals exhibited efficient signal transduction, survival, and proliferation, even at low IL-15 concentrations.
  • These findings contradict previous reports of a long-lasting global deficit in T-cell IL-15 responsiveness post-IM.

Conclusions:

  • Remote Epstein-Barr virus infection does not appear to cause a persistent impairment in T-cell IL-15Ralpha expression or function.
  • The immune balance following IM may not be characterized by a long-term global deficit in T-cell IL-15 responsiveness.
  • These results offer new insights into the long-term immune sequelae of infectious mononucleosis.

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