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Cytokine profiles in children with primary Epstein–Barr virus infection
Author(s) -
Wada Taizo,
Muraoka Masahiro,
Yokoyama Tadafumi,
Toma Tomoko,
Kanegane Hirokazu,
Yachie Akihiro
Publication year - 2013
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.24480
Subject(s) - mononucleosis , hemophagocytic lymphohistiocytosis , immunology , medicine , pathogenesis , neopterin , virus , epstein–barr virus , immune system , interferon , cytokine , epstein–barr virus infection , virology , tumor necrosis factor alpha , disease , pathology
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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