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NK‐cell repertoire is feasible for diagnosing Epstein–Barr virus‐infected NK‐cell lymphoproliferative disease and evaluating the treatment effect
Author(s) -
Sawada Akihisa,
Sato Emiko,
Koyama Maho,
Higuchi Banryoku,
Kusuki Shigenori,
Kim Ji Yoo,
Takeshita Yasufumi,
Sakata Akifumi,
Sakata Naoki,
Okamura Takayuki,
Yasui Masahiro,
Inoue Masami,
Kawa Keisei
Publication year - 2006
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.20659
Subject(s) - biology , lymphoproliferative disorders , immunology , virology , virus , lymphoma , epstein–barr virus
Abstract Epstein–Barr virus (EBV) occasionally infects T and NK cells and causes EBV‐infected T/NK‐cell lymphoproliferative disease (LPD), which comprises chronic active EBV infection, EBV‐associated hemophagocytic syndrome, mosquito allergy, hydroa vacciniforme, aggressive NK‐cell leukemia, and NK/T‐cell lymphoma. The diagnosis is proven by the monoclonal proliferation of EBV‐infected T or NK cells, which is a time‐consuming and complicated method. T‐cell monoclonality is helpful for the screening of EBV‐infected T‐cell LPD in patients with EBV‐genome burden and is easily shown with T‐cell‐receptor rearrangement or the T‐cell repertoire, whereas NK‐cell monoclonality is difficult to prove due to its lacking such rearranged receptors. We investigated a set of killer immunoglobulin‐like receptors (KIRs) and also CD94‐NKG2 heterodimers on NK cells, namely the NK‐cell repertoire. Skewed repertoires were seen in all patients with EBV‐infected NK‐cell LPD, but not in any patients with EBV‐infected T‐cell LPD and were restored only after successful treatment. The normal KIR repertoire is variable for each individual and it seems difficult to detect minimal residual EBV‐infected lymphocytes. However, the NK‐cell repertoire is feasible for identifying EBV‐infected NK‐cell LPD and evaluating the treatment effect. Am. J. Hematol. 81:576–581, 2006. © 2006 Wiley‐Liss, Inc.