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Transcription factor IRF8 orchestrates the adaptive natural killer cell response

ABSTRACT: Transcription factor IRF8 orchestrates the adaptive natural killer cell response

PROVIDER: PRJNA449549 | ENA |

REPOSITORIES: ENA

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Transcription factor IRF8 orchestrates the adaptive natural killer cell response

Project description:Natural killer (NK) cells are innate lymphocytes that have been recently appreciated to display features of adaptive immunity in response to viral infection. Biallelic mutations in the IRF8 gene have been reported to cause familial NK cell deficiency and susceptibility to severe viral infection in humans; however, the precise role of this transcription factor in regulating NK cell function remained unknown. Here, we show that IRF8 is required in a cell-intrinsic manner for NK cell-mediated protection against mouse cytomegalovirus (MCMV) infection. During exposure to MCMV, IRF8 is robustly upregulated in NK cells by IL-12 and STAT4, which promotes epigenetic remodeling of the Irf8 locus. Moreover, IRF8 facilitates the proliferative burst of virus-specific NK cells by promoting expression of a suite of DNA replication and cell cycle genes, and directly regulating Zbtb32, a master regulator of NK cell proliferation during viral challenge. These results identify a novel function and cell-type specific regulation for IRF8 in host antiviral immunity, and provide a mechanistic understanding of virus susceptibility in patients with IRF8 mutations.

2018-05-16 | GSE112948 | GEO

Transcription Factor IRF8 Orchestrates the Adaptive Natural Killer Cell Response.

Project description:Natural killer (NK) cells are innate lymphocytes that display features of adaptive immunity during viral infection. Biallelic mutations in IRF8 have been reported to cause familial NK cell deficiency and susceptibility to severe viral infection in humans; however, the precise role of this transcription factor in regulating NK cell function remains unknown. Here, we show that cell-intrinsic IRF8 was required for NK-cell-mediated protection against mouse cytomegalovirus infection. During viral exposure, NK cells upregulated IRF8 through interleukin-12 (IL-12) signaling and the transcription factor STAT4, which promoted epigenetic remodeling of the Irf8 locus. Moreover, IRF8 facilitated the proliferative burst of virus-specific NK cells by promoting expression of cell-cycle genes and directly controlling Zbtb32, a master regulator of virus-driven NK cell proliferation. These findings identify the function and cell-type-specific regulation of IRF8 in NK-cell-mediated antiviral immunity and provide a mechanistic understanding of viral susceptibility in patients with IRF8 mutations.

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Methylation in Adaptive Natural Killer cells after exposure to NKG2C agonist antibodies for 7 days

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Divergent role for STAT5 in the adaptive responses of natural killer cells

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Expression profiling of Natural killer B cells

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Divergent role for STAT5 in the adaptive responses of natural killer cells

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