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Xbp1s controls IL-15-mediated natural killer cell survival and function by regulating Pim2 and Tbet

ABSTRACT: Xbp1s controls IL-15-mediated natural killer cell survival and function by regulating Pim2 and Tbet

PROVIDER: PRJNA780404 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16946378.fastq.gz	Fastqsanger.gz
	SRR16946379.fastq.gz	Fastqsanger.gz
	SRR16946380.fastq.gz	Fastqsanger.gz
	SRR16946381.fastq.gz	Fastqsanger.gz
	SRR16946382.fastq.gz	Fastqsanger.gz

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Similar Datasets

Xbp1s controls IL-15-mediated natural killer cell survival and function by regulating Pim2 and Tbet

Project description:We previously reported that X-Box Binding Protein 1 (Xbp1s), an essential transcriptional factor downstream of IL-15 and Akt signaling, controls cell survival and effector function in human natural killer (NK) cells. However, the mechanisms by which Xbp1s regulates NK cell survival and function remains unknown. In this study, by using Xbp1s conditional knock-out (KO) mice, we found that Xbp1s is critical for IL-15-mediated NK cell survival but not proliferation in vitro and in vivo. Mechanically, Xbp1s regulates homeostatic NK cell survival through targeting Pim2, a critical anti-apoptotic gene. Pim2 in turn stabilizes Xbp1s protein through phosphorylation at Thr58. Xbp1s enhances NK cell effector function and anti-tumor immunity via recruitment of Tbet to the promoter region of Ifng. Collectively, our findings reveal an important role of IL-15–Xbp1s signaling in NK cell survival and effector function.

2022-12-31 | GSE188796 | GEO

An XBP1s-PIM-2 positive feedback loop controls IL-15-mediated survival of natural killer cells

Project description:We previously reported that XBP1s, an essential transcription factor downstream of IL-15 and AKT signaling, controls cell survival and effector functions of human natural killer (NK) cells. However, the precise mechanisms remain unknown. In this study, by using XBP1 conditional knock-out mice, we found that XBP1s is critical for IL-15-mediated NK cell survival but not proliferation in vitro and in vivo. Mechanistically, XBP1s regulates homeostatic NK cell survival through targeting PIM-2, a critical anti-apoptotic gene, which in turn stabilizes XBP1s protein by phosphorylating it at Thr58. In addition, XBP1s enhances the effector functions and anti-tumor immunity of NK cells by recruiting T-bet to the promoter region of Ifng. Collectively, our findings identify a previously unknown mechanism by which IL-15–XBP1s signaling regulates the survival and effector functions of NK cells.

2022-12-31 | GSE218543 | GEO

An XBP1s-PIM-2 positive feedback loop controls IL-15-mediated survival of natural killer cells

Project description:An XBP1s-PIM-2 positive feedback loop controls IL-15-mediated survival of natural killer cells

| PRJNA904273 | ENA

An XBP1s-PIM-2 positive feedback loop controls IL-15-mediated survival of natural killer cells.

Project description:Spliced X-box-binding protein 1 (XBP1s) is an essential transcription factor downstream of interleukin-15 (IL-15) and AKT signaling, which controls cell survival and effector functions of human natural killer (NK) cells. However, the precise mechanisms, especially the downstream targets of XBP1s, remain unknown. In this study, by using XBP1 conditional knockout mice, we found that XBP1s is critical for IL-15-mediated NK cell survival but not proliferation in vitro and in vivo. Mechanistically, XBP1s regulates homeostatic NK cell survival by targeting PIM-2, a critical anti-apoptotic gene, which in turn stabilizes XBP1s protein by phosphorylating it at Thr58. In addition, XBP1s enhances the effector functions and antitumor immunity of NK cells by recruiting T-bet to the promoter region of Ifng. Collectively, our findings identify a previously unknown mechanism by which IL-15-XBP1s signaling regulates the survival and effector functions of NK cells.

| S-EPMC10216801 | biostudies-literature

Tbet-Eomes

Project description:Tbet-Eomes

| PRJNA706657 | ENA

Expression data from Tbet+ and Tbet- Memory B cells

Project description:The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was imÂportant even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages. NaÃ¯ve, Tbet+, and Tbet- Memory B cells were assayed for gene expression Tbet GFP reporter mice were infected with LCMV clone 13, and target B cell populations were sorted from splenocytes at day 10 post-infection

2016-08-01 | E-GEOD-81189 | biostudies-arrayexpress

XBP1s cutnrun

Project description:XBP1s cutnrun

| PRJNA949270 | ENA

XBP1s cutnrun

Project description:XBP1s cutnrun

| PRJNA887070 | ENA

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.

2016-05-17 | E-GEOD-80063 | biostudies-arrayexpress

Tbet promotes CXCR6 expression in immature natural killer cells and natural killer cell egress from the bone marrow.

Project description:Tbet-deficient mice have reduced natural killer (NK) cells in blood and spleen, but increased NK cells in bone marrow and lymph nodes, a phenotype that is thought to be the result of defective migration. Here, we revisit the role of Tbet in NK cell bone marrow egress. We definitively show that the accumulation of NK cells in the bone marrow of Tbet-deficient Tbx21-/- animals occurs because of a migration defect and identify a module of genes, co-ordinated by Tbet, which affects the localization of NK cells in the bone marrow. Cxcr6 is approximately 125-fold underexpressed in Tbx21-/- , compared with wild-type, immature NK cells. Immature NK cells accumulate in the bone marrow of CXCR6-deficient mice, and CXCR6-deficient progenitors are less able to reconstitute the peripheral NK cell compartment than their wild-type counterparts. However, the CXCR6 phenotype is largely confined to immature NK cells, whereas the Tbet phenotype is present in both immature and mature NK cells, suggesting that genes identified as being more differentially expressed in mature NK cells, such as S1pr5, Cx3cr1, Sell and Cd69, may be the major drivers of the phenotype.

| S-EPMC7450165 | biostudies-literature

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