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Department of Microbiology, National Public Health Institute, Helsinki, Finland
Correspondence
Jukka Sirén
jukka.siren{at}ktl.fi
NK cells participate in innate immune responses by secreting gamma interferon (IFN-
) and by destroying virus-infected cells. Here the interaction between influenza A or Sendai virus-infected macrophages and NK cells has been studied. A rapid, cellcell contact-dependent production of IFN-
from NK cells cultured with virus-infected macrophages was observed. Expression of the MHC class I-related chain B (MICB) gene, a ligand for NK cell-activating receptor NKG2D, was upregulated in virus-infected macrophages suggesting a role for MICB in the activation of the IFN-
gene in NK cells. IL12R
2, IL18R and T-bet mRNA synthesis was enhanced in NK cells cultured with virus-infected macrophages. Upregulation of these genes was dependent on macrophage-derived IFN-
. In contrast to IL12R
2, expression of WSX-1/TCCR, a receptor for IL27, was reduced in NK cells in response to virus-induced IFN-
. In conclusion, these results show that virus-infected macrophages activate NK cells via cytokines and direct cellular interactions and further emphasize the role of IFN-
in the activation of innate immunity.
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