Cytokine and contact-dependent activation of natural killer cells by influenza A or Sendai virus-infected macrophages Sirén, Jukka and Sareneva, Timo and Pirhonen, Jaana and Strengell, Mari and Veckman, Ville and Julkunen, Ilkka and Matikainen, Sampsa,, 85, 2357-2364 (2004), doi = https://doi.org/10.1099/vir.0.80105-0, publicationName = Microbiology Society, issn = 0022-1317, abstract= NK cells participate in innate immune responses by secreting gamma interferon (IFN-γ) 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, cell–cell contact-dependent production of IFN-γ 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-γ gene in NK cells. IL12Rβ2, 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-α. In contrast to IL12Rβ2, expression of WSX-1/TCCR, a receptor for IL27, was reduced in NK cells in response to virus-induced IFN-α. 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-α in the activation of innate immunity., language=, type=