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

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

PROVIDER: PRJNA598546 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10814011_1.fastq.gz	Fastqsanger.gz
	SRR10814011_2.fastq.gz	Fastqsanger.gz
	SRR10814012_1.fastq.gz	Fastqsanger.gz
	SRR10814012_2.fastq.gz	Fastqsanger.gz
	SRR10814013_1.fastq.gz	Fastqsanger.gz

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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.

2020-12-27 | GSE142821 | GEO

Critical functions for STAT5 tetramers in the maturation and survival of natural killer cells

Project description:Interleukin-15 (IL-15) is essential for the development and maintenance of natural killer (NK) cells. IL-15 activates STAT5 proteins, which can form dimers or tetramers. We previously found that NK cell numbers are decreased in Stat5a-Stat5b tetramer-deficient double knockin (DKI) mice, but the mechanism was not investigated. Here we show that STAT5 dimers are sufficient for NK cell development, whereas STAT5 tetramers mediate NK cell maturation and the expression of maturation-associated genes. Unlike the defective proliferation of Stat5 DKI CD8+ T cells, Stat5 DKI NK cells have normal proliferation to IL-15 but are susceptible to death upon cytokine withdrawal, with lower Bcl2 and increased active caspases. These findings underscore the importance of STAT5 tetramers in maintaining NK cell homeostasis. Moreover, defective STAT5 tetramer formation could represent a cause of NK cell immunodeficiency, and interrupting STAT5 tetramer formation might serve to control NK leukaemia.

2017-09-19 | GSE101470 | GEO

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

Project description:Natural Killer cells from cytomegalovirus positive individuals (i.e. adaptive NK) where cultured for seven days with either control antibody, an NKG2C agonist antibody, or an antibody agonist to NKG2C and NKG2A

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Transcription factor IRF8 orchestrates the adaptive natural killer cell response

Project description: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 roles of this transcription factor and its upstream cytokines interleukin-2 (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 role for STAT5 signaling in promoting an optimal anti-viral NK cell response.

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Expression profiling of Natural killer B cells

Project description:Investigation of global gene expression levels between B cells, Natural killer cells and Natural killer B cells Gene expression profiling using sorted B cells, Natural killer cells and Natural killer B cells from WT mouse spleen. Total RNA extracted from WT cells were quantified by the NanoDrop ND-1000 and RNA integrity was assessed by standard denaturing agarose gel electrophoresis. The sample preparation and microarray hybridization were performed based on the NimbleGenâs standard protocols.

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Expression profiling of Natural killer B cells

Project description:Investigation of global gene expression levels between B cells, Natural killer cells and Natural killer B cells

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Project description:Comparing global gene expression of neonatal and adult natural killer cells to determine if differences in gene expression suggest that different developmental pathways during hematopoiesis are followed in the fetal and adult mouse to produce mature natural killer cells.

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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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Innate-like functions of natural killer T cell subsets result from highly divergent gene programs

Project description:Innate-like functions of natural killer T cell subsets result from highly divergent gene programs

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