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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.

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Transcription Factor IRF8 Orchestrates the Adaptive Natural Killer Cell Response.

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

Project description:Natural killer (NK) cells are innate lymphocytes with the capacity to elicit adaptive features, including clonal expansion and immunological memory. Because signal transducer and activator of transcription 5 (STAT5) is essential for NK cell development, the role of this transcription factor and its upstream cytokines IL-2 and IL-15 during infection have not been carefully investigated. In this study, we investigate how STAT5 regulates transcription during viral infection. We demonstrate that STAT5 is induced in NK cells by IL-12 and STAT4 early after infection, and that partial STAT5 deficiency results in a defective capacity of NK cells to generate long-lived memory cells. Furthermore, we find a functional dichotomy of IL-2 and IL-15 signaling outputs during viral infection, whereby both cytokines drive clonal expansion, but only IL-15 is required for memory NK cell survival. We thus highlight a novel role for STAT5 signaling in promoting an optimal antiviral NK cell response.

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