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Natural killer cell proliferation requires canonical IRE1 function during viral infection

ABSTRACT: Natural killer cell proliferation requires canonical IRE1 function during viral infection

PROVIDER: PRJNA992477 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25194900_1.fastq.gz	Fastqsanger.gz
	SRR25194900_2.fastq.gz	Fastqsanger.gz
	SRR25194901_1.fastq.gz	Fastqsanger.gz
	SRR25194901_2.fastq.gz	Fastqsanger.gz
	SRR25194902_1.fastq.gz	Fastqsanger.gz

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Natural killer cell proliferation requires canonical IRE1 function during viral infection (RNA-Seq)

Project description:Natural killer cell proliferation requires canonical IRE1 function during viral infection (RNA-Seq)

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Natural killer cell proliferation requires canonical IRE1 function during viral infection (CITE-Seq)

Project description:Natural killer cell proliferation requires canonical IRE1 function during viral infection (CITE-Seq)

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Natural killer cell proliferation requires canonical IRE1 function during viral infection (CITE-Seq)

Project description:The unfolded protein response (UPR) aims to restore ER homeostasis under conditions of high protein folding load, a function primarily serving secretory cells. Additional, non-canonical UPR functions have recently been unraveled in immune cells. We addressed the function of the inositol-requiring-enzyme 1 (IRE1) signaling branch of the UPR in NK cells in homeostasis and microbial challenge. Cell-intrinsic compound deficiency (DKO) of IRE1 and its downstream transcription factor XBP1 in NKp46 + NK cells, did not affect basal NK cell homeostasis, or overall outcome of viral MCMV infection. However, mixed bone marrow chimeras revealed a competitive advantage in the proliferation of IRE1 sufficient Ly49H + NK cells after viral infection. CITE-Seq analysis confirmed strong induction of IRE1 early upon infection, concomitant with the activation of a canonical UPR signature. Therefore, we conclude that cell-intrinsic IRE1/XBP1 activation is required for NK cell proliferation early upon viral infection, as part of a canonical UPR response.

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Natural killer cell proliferation requires canonical IRE1 function during viral infection (RNA-Seq)

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Natural killer cell proliferation requires canonical IRE1 function during viral infection

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IRE1-dependent transcriptional change under a canonical endoplasmic-reticulum stressing stimulus and upon diauxic shift in Saccharomyces cerevisiae cells

Project description:Ire1 is an endoplasmic reticulum (ER)-located transmembrane protein that triggers the unfolded protein response. I recently noticed that Ire1 is activated not only in response to ER accumulation of unfolded proteins but also alongside diauxic shift in yeast Saccharomyces cerevisiae cells. I thus asked how different the Ire1-target genes upon two distinct scenes, a canonical ER -stressing stimuli and diauxic shift. Thus NGS transcriptome analysis was performed by using IRE1+ and ire1-delta mutant yeast cells under these conditions.

2019-03-01 | E-MTAB-6923 | biostudies-arrayexpress

The IRE1-XBP1 pathway promotes natural killer cell responses against viral infection and cancer by regulation of c-Myc

Project description:Natural killer (NK) cells are critical mediators of host immunity against infectious disease and cancer. The intrinsic regulators of NK cells are not fully understood. Here, we demonstrate that the ER stress sensor inositol-requiring enzyme 1 (IRE1α) and its substrate transcription factor X-box-binding protein 1 (XBP1) critically drive NK cell-mediated responses against viral infection and tumors. IRE1α and XBP1 were essential for the robust expansion of activated mouse and human NK cells. Transcriptome analysis revealed the transcription factor c-Myc as a novel and direct target of XBP1 for downstream regulation of NK cell proliferation. Genetic ablation or pharmaceutical blockade of IRE1α downregulated c-Myc, whereas overexpression of XBP1 resulted in c-Myc hyperactivation. NK cells lacking c-Myc demonstrated a functional deficit comparable to IRE1α or XBP1 deficiency. Overall, our study identifies a novel IRE1-XBP1-cMyc axis in NK cell immunity, providing new insight into the host immune response against infection and cancer.

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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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