Cytokine profiles in children with primary Epstein–Barr virus infection

Authors

  • Taizo Wada MD, PhD,

    Corresponding author
    1. Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan
    • Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, 13-1 Takaramachi, Kanazawa 920-8641, Japan.
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  • Masahiro Muraoka MD,

    1. Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan
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  • Tadafumi Yokoyama MD, PhD,

    1. Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan
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  • Tomoko Toma MD, PhD,

    1. Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan
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  • Hirokazu Kanegane MD, PhD,

    1. Department of Pediatrics, Graduate School of Medicine and Pharmaceutical Science, University of Toyama, Toyama, Japan
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  • Akihiro Yachie MD, PhD

    1. Department of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan
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  • Conflict of interest: Nothing to declare.

Abstract

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.

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