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J Gen Virol 85 (2004), 2357-2364; DOI 10.1099/vir.0.80105-0

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© 2004 Society for General Microbiology

Cytokine and contact-dependent activation of natural killer cells by influenza A or Sendai virus-infected macrophages

Jukka Sirén, Timo Sareneva, Jaana Pirhonen, Mari Strengell, Ville Veckman, Ilkka Julkunen and Sampsa Matikainen

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-{gamma}) 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-{gamma} 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-{gamma} gene in NK cells. IL12R{beta}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-{alpha}. In contrast to IL12R{beta}2, expression of WSX-1/TCCR, a receptor for IL27, was reduced in NK cells in response to virus-induced IFN-{alpha}. 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-{alpha} in the activation of innate immunity.




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