Conflict of interest: Nothing to declare.
Cytokine profiles in children with primary Epstein–Barr virus infection†
Article first published online: 4 FEB 2013
Copyright © 2013 Wiley Periodicals, Inc.
Pediatric Blood & Cancer
Volume 60, Issue 7, pages E46–E48, July 2013
How to Cite
Wada, T., Muraoka, M., Yokoyama, T., Toma, T., Kanegane, H. and Yachie, A. (2013), Cytokine profiles in children with primary Epstein–Barr virus infection. Pediatr. Blood Cancer, 60: E46–E48. doi: 10.1002/pbc.24480
- Issue published online: 22 MAY 2013
- Article first published online: 4 FEB 2013
- Manuscript Accepted: 27 DEC 2012
- Manuscript Received: 11 NOV 2012
- Hokkoku Gan Kikin, Kanazawa
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Ministry of Health, Labour, and Welfare of Japan, Tokyo
- Epstein–Barr virus;
- hemophagocytic lymphohistiocytosis;
- infectious mononucleosis
Primary Epstein–Barr virus (EBV) infection causes infectious mononucleosis and hemophagocytic lymphohistiocytosis (HLH) in children, where EBV infects B and CD8+ T cells, respectively. We measured pro-inflammatory and anti-inflammatory cytokines in both diseases. Significantly higher concentrations of various mediators, including interferon-γ, neopterin, interleukin (IL)-6, IL-10, IL-18, and heme oxygenase-1, were observed in EBV-HLH. Because of their similarity to the profile of familial HLH, this profile was likely a consequence of HLH, but not ectopic infection. TNF-α levels were elevated in both diseases. Elevation of those mediators may contribute to the disease pathogenesis of EBV-HLH by activating and inhibiting host immune responses. Pediatr Blood Cancer 2013; 60: E46–E48. © 2013 Wiley Periodicals, Inc.