Interferon-γ prevents apoptosis in Epstein-Barr virus-infected natural killer cell leukemia in an autocrine fashion

Shin Ichi Mizuno, Koichi Akashi, Koichi Ohshima, Hiromi Iwasaki, Toshihiro Miyamoto, Naoyuki Uchida, Tsunefumi Shibuya, Mine Harada, Masahiro Kikuchi, Yoshiyuki Niho

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)

Abstract

The significant function of cytokines includes maintenance of cell survival as well as induction of cell differentiation and/or proliferation. We demonstrate here that interferon-γ (IFN-γ) plays a role for progression of Epstein-Barr virus (EBV)-infected natural killer cell leukemia (NK leukemia) through maintaining cell survival. NK leukemia cells obtained from 7 patients had clonal episomal forms of EBV, indicating that the leukemic cells were of clonal origin. Although normal NK cells constitutively expressed Bcl-2, the EBV-infected NK leukemia cells lacked endogenous Bcl-2 expression and were hypersensitive to apoptosis in vitro. The addition of IFN-γ to the culture significantly inhibited their spontaneous apoptosis without inducing cell proliferation or upregulation of Bcl-2. The NK leukemia cells constitutively secreted IFN-γ, and the patients' sera contained a high concentration of IFN-γ, levels that were high enough to prevent NK leukemia cells from apoptosis. Bcl-X(L) was not involved in the IFN-γ-induced NK leukemia cell survival. These data suggest that the acquisition of IFN-γ- mediated autocrine survival signals, other than Bcl-2 or BCL-X(L), might be important for the development of EBV-infected NK leukemia.

Original languageEnglish
Pages (from-to)3494-3504
Number of pages11
JournalBlood
Volume93
Issue number10
DOIs
Publication statusPublished - May 15 1999
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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