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Blood, 1 July 2006, Vol. 108, No. 1, pp. 11-18.
Prepublished online as a Blood First Edition Paper on March 16, 2006; DOI 10.1182/blood-2006-01-0144.
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Submitted January 12, 2006
Accepted February 11, 2006
EBV-associated mononucleosis leads to long-term global deficit in T cell responsiveness to IL-15
Delphine Sauce, Martin Larsen, S John Curnow, Alison M Leese, Paul A Moss, Andrew D Hislop, Michael Salmon, and Alan B Rickinson*
University of Birmingham, CRUK Institute for Cancer Studies, Birmingham, United Kingdom
University of Birmingham, MRC Centre for Immune Regulation, Birmingham, United Kingdom
* Corresponding author; email: A.B.Rickinson{at}bham.ac.uk.
In mice the interleukins (IL) 7 and 15 are involved in T cell homeostasis and the maintenance of immunologic memory. Here we follow virus-induced responses in infectious mononucleosis (IM) patients from primary Epstein-Barr virus (EBV) infection into long-term virus carriage, monitoring IL-7 and IL-15 receptor (IL-R) expression by antibody staining and cytokine responsiveness by STAT5 phosphorylation and in vitro proliferation. Expression of IL-7R was lost from all CD8+ T cells, including EBV epitope-specific populations, during acute IM. Thereafter expression recovered quickly on total CD8+ cells but slowly and incompletely on EBV-specific memory cells. Expression of IL-15R was also lost in acute IM and remained undetectable thereafter not just on EBV-specific CD8+ populations but on the whole peripheral T and NK cell pool. This deficit, correlating with defective IL-15 responsiveness in vitro, was consistently observed in patients up to 14 years post-IM but not in patients after cytomegalovirus (CMV)-associated mononucleosis, nor in healthy EBV carriers with no history of IM, nor in EBV-naive individuals. By permanently scarring the immune system, symptomatic primary EBV infection provides a unique cohort of patients through which to study the effects of impaired IL-15 signalling on human lymphocyte functions in vitro and in vivo.
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