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Induction of CD16 + CD56 bright NK Cells with Antitumour Cytotoxicity not only from CD16 − CD56 bright NK Cells but also from CD16 − CD56 dim NK Cells
Author(s) -
Takahashi E.,
Kuranaga N.,
Satoh K.,
Habu Y.,
Shinomiya N.,
Asano T.,
Seki S.,
Hayakawa M.
Publication year - 2007
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2006.01883.x
Subject(s) - cd16 , nkg2d , interleukin 12 , natural killer cell , microbiology and biotechnology , interleukin 21 , lymphokine activated killer cell , janus kinase 3 , biology , cytotoxic t cell , immunology , antigen , cd3 , cd8 , in vitro , biochemistry
The aim of this study was to examine the effect of cytokines on different subsets of NK cells, while especially focusing on CD16 − CD56 dim cells and CD16 − CD56 bright cells. When human peripheral blood mononuclear cells (PBMC) were cultured with a combination of IL‐2, IL‐12 and IL‐15 for several days, a minor population of CD56 bright NK cells expanded up to 15%, and also showed potent cytotoxicities against various cancer cells. Sorting experiments revealed that unconventional CD16 − CD56 + NK cells (CD16 − CD56 dim NK cells and CD16 − CD56 bright NK cells, both of which are less than 1% in PBMC) much more vigorously proliferated after cytokine stimulation, whereas predominant CD16 + CD56 dim NK cells proliferated poorly. In addition, many of the resting CD16 − CD56 bright NK cells developed into CD16 + CD56 bright NK cells, and CD16 − CD56 dim NK cells developed into CD16 − CD56 bright NK cells and also further into CD16 + CD56 bright NK cells by the cytokines. CSFE label experiments further substantiated the proliferation capacity of each subset and the developmental process of CD16 + CD56 bright NK cells. Both CD16 − CD56 dim NK cells and CD16 − CD56 bright NK cells produced large amounts of IFN‐ γ and Fas‐ligands. The CD16 + CD56 bright NK cells showed strong cytotoxicities against not only MHC class I (−) but also MHC class I (+) tumours regardless of their expression of CD94/NKG2A presumably because they expressed NKG2D as well as natural cytotoxicity receptors. The proliferation of CD16 + CD56 bright NK cells was also induced when PBMC were stimulated with penicillin‐treated Streptococcus pyogenes , thus suggesting their role in tumour immunity and bacterial infections.