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Transcription factor IRF4 deficiency in NK precursors pre-determines epigenetic changes in mature NK cells

ABSTRACT: Transcription factor IRF4 deficiency in NK precursors pre-determines epigenetic changes in mature NK cells

PROVIDER: PRJNA1195047 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31635149_1.fastq.gz	Fastqsanger.gz
	SRR31635149_2.fastq.gz	Fastqsanger.gz
	SRR31635150_1.fastq.gz	Fastqsanger.gz
	SRR31635150_2.fastq.gz	Fastqsanger.gz
	SRR31635151_1.fastq.gz	Fastqsanger.gz

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Transcription factor IRF4 deficiency in NK precursors pre-determines epigenetic changes in mature NK cells

Project description:To explore whether IRF4 deficiency determine the epigenetic changes of mature NK cells is at the NKP cell stage, ATAC-seq was performed to analyze chromatin accessibility of NK cells from spleen WT, Irf4-/-, Irf4flox/flox and Ncr1cre+/-Irf4flox/flox mice.

2024-12-11 | GSE283690 | GEO

Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in quiescent mature B cells.

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Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation and stimulated with anti-CD40 antibodies and IL-4

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in CD40+IL-4 activated mature B cells. B cells from 12-week old irf4-/- and irf4+/+ littermate mice were isolated by magnetic depletion of non-B cells from splenic mononuclear cells and cultures with mitogens in vitro. RNA was isolated. Labeled cRNA was hybridized to microarrays and genes specifically expressed in irf4-/- vs. irf4+/+ samples.

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Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation and stimulated with anti-CD40 antibodies and IL-4

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in CD40+IL-4 activated mature B cells.

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Gene expression profile of NK cells from Wilde type C57BL/6 (B6) and Irf4-/- injected with B16-F10 post 20 days or not [bulk RNA-seq]

Project description:IRF4 deficient NK cells displayed more resistant to exhaustion during B16-F10 metastasis, to investigate how IRF4 deletion enhances the resistance of NK cells to exhaustion, we sorted NK cells from WT and Irf4-/- mice ingected with B16-F10 or not for RNA-seq

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Transcription profiling by array of mouse irf4 knockout mature splenic B cells against wild type controls from littermates

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in quiescent mature B cells. B cells from 12-week old irf4-/- and irf4+/+ littermate mice were isolated by magnetic depletion of non-B cells from splenic mononuclear cells. RNA was isolated. Labeled cRNA was hybridized to microarrays and genes specifically expressed in irf4-/- vs. irf4+/+ samples.

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Gene expression profile at single cell level of NKP cells from Wilde type C57BL/6 (B6) and Irf4-/- mice bone marrow [scRNA-seq]

Project description:IRF4 deficiency affect the development of mature NK cells, we used single cell RNA sequencing(scRNA-seq) to investigate the changes in NKP cells resulting from the deletion of IRF4.

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Gene expression profiling of NKG2C+ NK cells generated from inflammatory CD34+DNAM-1brCXCR4+ and Lin-CD34- CD16+CD56- blood precursors

Project description:There is limited knowledge on the origin and development of the ample spectrum of human NK cells, particularly of specialized NK subsets. Here, we characterized the NK cell progeny of CD34+DNAM-1bright CXCR4+ precursors that reside in healthy bone marrow and circulate in the peripheral blood (PB) of patients with chronic infections/inflammation. including HIV, HCV or HCMV reactivation after HSC transplantation. Unlike conventional CD34+ precursors they rapidly differentiated in vitro into cytotoxic, IFNγ-secreting CD94/NKG2C+KIR+CD57+ maturing NK cell progenies with HCMV-inhibiting activity. Progeny characterization led also to identification of an additional new PB Lin-CD56-CD16+ precursor giving rise to the same CD94/NKG2C+KIR+CD57+ maturing NK cell progenies. Microarray analysis of NK cell progenies revealed a signature compatible with maturing adaptive NK cells. In vivo circulation of multiple common lymphocyte precursors with rapid development to NKG2C+ NK cell progeny is steadily occurring and may thus be a crucial resource for the prompt control of HCMV. We used microarray to compare the transcriptional profiles of human NKG2C+ NK cells derived from i) CD34+DNAM1brightCXCR4+ precursors, ii) Lin-CD34-CD16+CD56- precursors, iii) peripheral blood.

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Control of nutrient uptake by IRF4 orchestrates innate immune memory - ChIP-seq

Project description:Natural Killer (NK) cells are innate cytotoxic lymphocytes with adaptive immune features, including antigen-specificity, clonal expansion, and memory. As such, NK cells share many transcriptional and epigenetic programs with their adaptive CD8+ T cell siblings. Various signals ranging from antigen, co-stimulation, and proinflammatory cytokines are required for optimal NK cell responses in mice and humans during virus infection; however, the integration of these signals remains unclear. In this study, we identified the transcription factor IRF4 as a signal integrator to coordinate the NK cell response during viral infection. Loss of IRF4 was detrimental to the expansion and differentiation of virus-specific NK cells. This defect was partially attributed to the inability of IRF4-deficient NK cells to uptake nutrients required for survival and memory generation. Altogether, these data suggest IRF4 is a signal integrator that acts as a secondary metabolic checkpoint to orchestrate the adaptive response of NK cells during viral infection.

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Control of nutrient uptake by IRF4 orchestrates innate immune memory - scRNA-seq

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