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Expression of epstein‐barr virus‐encoded growth‐transformation‐associated proteins in lymphoproliferations of bone‐marrow transplant recipients
Author(s) -
Gratama Jan W.,
Zutter Mary M.,
Minarovits Janos,
Oosterveer Maria A. P.,
Donnall Thomas E.,
Klein George,
Ernberg Ingemar
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910470205
Subject(s) - immunosurveillance , ctl* , epstein–barr virus , biology , virus , virology , antigen , cytotoxic t cell , bone marrow , immunology , cancer research , in vitro , immune system , cd8 , genetics
The expression of Epstein‐Barr virus (EBV)‐encoded, growth‐transformation‐associated proteins was studied in lymphoproliferations of 9 allogeneic bone‐marrow transplant (BMT) recipients. Immunoblots of cell lysates were probed with polyspecific and monospecific antisera directed against EBNA I, 2, 3 and 6, and the membrane protein LMP. All tumors expressed EBNA I and LMP. EBNA 2 was detected in the tumors of 8 patients, and EBNA 3 and 6 in the tumors of 5 patients. The LMP regulatory sequences, 5′ of the LMP gene, were totally unmethylated in all 7 cases, while the coding sequences of LMP and EBNA 2 were more methylated in CpG dinucleotides. EBV‐transformed lymphoblastoid cell lines (LCL) express EBNA I to 6 and LMP; in contrast, Burkitt lymphomas express only EBNA I. In vitro experiments have shown that EBNA 2, 3 and LMP can generate targets for cytotoxic T cells (CTL). These combined observations are consistent with the hypothesis that the EBV‐associated lym‐phoprod'ferative disease of the BMT recipients escapes CTL‐mediated rejection due to the failure of host immunosurveillance rather than to the down‐regulation of immunogenic EBV‐encoded antigens.