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BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[RNA]

ABSTRACT: BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[RNA]

PROVIDER: PRJNA1143026 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30101456_1.fastq.gz	Fastqsanger.gz
	SRR30101456_2.fastq.gz	Fastqsanger.gz
	SRR30101457_1.fastq.gz	Fastqsanger.gz
	SRR30101457_2.fastq.gz	Fastqsanger.gz
	SRR30101458_1.fastq.gz	Fastqsanger.gz

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BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[RNA]

Project description:We identified BATF as a core transcription factor and the main mediator of this NK cell dysfunction in AML. our findings reveal a previously unidentified mechanism of NK immune evasion in AML manifested by epigenetic rewiring and inactivation of NK cells by myeloid blasts.  This work highlights the importance of using healthy allogeneic NK cells as adoptive cell therapy to treat patients with myeloid malignancies combined with strategies aimed at preventing the dysfunction by targeting the TGF-b pathway or BATF

2024-08-31 | GSE273750 | GEO

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Project description:BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[CUT&RUN]

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BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML[ATAC-seq]

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BATF knockout B cells

Project description:compare wild type and Batf-/- B cells activated for 0 1 or 2 days in vitro. WT or Batf deficient B cells were activated in vitro with LPS for 1 or 2 days, or left untreated. B cells were purified by MACS and activated, harvested and prepped for affymetrix gene expression profiling.

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Transcription profiling by array of mouse M1 cells expressing Batf targeting siRNA or control siRNA and treated with leukemia inhibitory factor to identify putative downstream targets of Batf

Project description:In order to identify putative downstream targets of Batf in M1 cells, a microarray analysis was performed. Briefly, M1/Neg-RNAi (expressing control siRNA with no mammalian target) and M1/Batf-RNAi cells (expressing Batf targeting siRNA) were seeded in M1 growth medium at a density of 3 X 105/ml in 100mm culture dishes. Six plates were plated for each cell type. Within each group, three were labeled as + LIF and treated with leukemia inhibitory factor (LIF) (5 ng/ml) for 6 hours the following day. After 6 hours, the cells were harvested from all plates individually and RNA prepared. 5 µg of total RNA from the three individual samples representing each subgroup (M1/Neg-RNAi + LIF, - LIF; M1/Batf-RNAi + LIF, - LIF) were combined into one pool of RNA. EJT001 represents sample "M1/Neg-RNAi, no LIF)"; EJT002 represents sample "M1/Neg-RNAi, with LIF)"; EJT003 represents sample "M1/Batf-RNAi, no LIF)"; EJT004 represents sample "M1/Batf-RNAi, with LIF)". The four pools of RNA were shipped to Genome Explorations, Inc. for analysis using Affymetrix GeneChip technology. The differentially regulated genes were identified both within each group (+ LIF compared to - LIF) and between 2 goups (M1/Neg-RNAi and M1/Batf-RNAi).

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Project description:Natural killer (NK) cells are innate lymphocytes that play a major role in immunosurveillance against tumor initiation and metastasis spread. Signals and checkpoints that regulate NK cell fitness and function in the tumor microenvironment are not well defined. Transforming grow factor (TGF)- is a recognized suppressor of NK cells that inhibits IL-15 dependent signaling events and induces cellular transdifferentiation, however the role of other SMAD signaling pathways in NK cells is unknown. We used a global, label-free proteomics approach to compare the protein expression profiles of NK cells in the presence of TGF-b or activin-A.

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