@article{mbs:/content/journal/jgv/10.1099/vir.0.80105-0, author = "Sirén, Jukka and Sareneva, Timo and Pirhonen, Jaana and Strengell, Mari and Veckman, Ville and Julkunen, Ilkka and Matikainen, Sampsa", title = "Cytokine and contact-dependent activation of natural killer cells by influenza A or Sendai virus-infected macrophages", journal= "Journal of General Virology", year = "2004", volume = "85", number = "8", pages = "2357-2364", doi = "https://doi.org/10.1099/vir.0.80105-0", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.80105-0", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", 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.", }