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Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells

ABSTRACT: Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells

PROVIDER: PRJNA627593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11594424_1.fastq.gz	Fastqsanger.gz
	SRR11594424_2.fastq.gz	Fastqsanger.gz
	SRR11594425_1.fastq.gz	Fastqsanger.gz
	SRR11594425_2.fastq.gz	Fastqsanger.gz
	SRR11594426_1.fastq.gz	Fastqsanger.gz

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Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells [RNA-seq]

Project description:T cell development is a complicatedly hierarchical process which is closely related with the chromatin activation and gene transcription. CD4+CD8+ double-positive (DP) thymocytes give rise to both conventional TCRαβ+ T cells and natural killer T cells, but they display different characteristics. Compared with conventional TCRαβ+ T cells, invariant natural killer T cells (iNKT cells) as the major population of NKT cells, are CD1d-restricted, recognize glycolipid antigens and rapidly exert effector functions after stimulation. However, the specific molecular mechanism of early iNKT cell development remain incompletely understood. Here the authors show that deletion of Chromatin assembly factor 1B (CHAF1b) remains the normal development of conventional TCRαβ+ T cell, but specifically impacts iNKT cell generation and completely impairs iNKT cell development from stage 0 with a PLZF independent way. This dysregulation is accompanied by a specific decrease in gene transcription of Vα14-Jα18, an impairment in TCR signaling and PLZF expression. Notably, ectopic expression of a transgenic Vα14-Jα18 TCR completely rescues these defects in Chaf1b-deficient iNKT cells. Moreover, cytokine secretion and anti-tumor activity are substantially maintained in Chaf1b-deficient iNKT cells with transgenic Vα14-Jα18 TCR. Our study identifies CHAF1b as a distinct regulator controls early development of iNKT cells via transcriptional regulation of Vα14-Jα18.

2021-05-21 | GSE149176 | GEO

Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells [ATAC-seq]

2021-05-21 | GSE149174 | GEO

Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells [RNA-seq]

Project description:Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells [RNA-seq]

| PRJNA627600 | ENA

Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells [ATAC-seq]

Project description:Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells [ATAC-seq]

| PRJNA627601 | ENA

Chromatin assembly factor 1B critically controls early development but not functional acquisition of iNKT cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-21 | GSE149177 | GEO

UTX controls lineage-specific epigenetic program of iNKT cells

Project description:iNKT cells are innate-like lymphocytes that protect against infection, autoimmune disease, and cancer. However, little is known about epigenetic regulation of iNKT cell development. Here, we show that the H3K27me3 histone demethylase UTX is an essential cell-intrinsic factor that controls an iNKT lineage specific gene expression program and epigenetic landscape in a demethylase activity dependent manner. UTX deficient iNKT cells exhibit impaired expression of iNKT signature genes due to a decrease in activation-associated H3K4me3 and an increase in repressive H3K27me3 marks within the promoters that UTX occupies. Notably, we identified JunB as a novel regulator of iNKT development that partners with UTX to establish an iNKT lineage specific gene expression program. Moreover, we demonstrate that UTX-mediated regulation of super-enhancer accessibility is a key mechanism for iNKT lineage commitment. These findings uncover how UTX regulates iNKT cell development through multiple epigenetic mechanisms.

2016-12-19 | GSE84015 | GEO

Analysis of transcriptomic profile of iNKT cells

Project description:The maintenance of tissue homeostasis is critically dependent on the function of tissue-resident lymphocytes, including lipid-reactive invariant natural killer T (iNKT) cells. iNKT cells have unique properties according to their tissues of residency, but if and how the tissue environment shapes their antigen specificity remains unknown. By analysing iNKT cells from tissues of mice and humans we demonstrate that their T cell receptor (TCR) repertoire is highly diverse and is distinct for iNKT cells resident in individual tissues resulting in differential lipid-antigen recognition. Within peripheral tissues, the TCR repertoire of iNKT cell recent thymic emigrants is different from that of mature cells, indicating that the iNKT population is shaped after their arrival to the tissues. Accordingly, in homeostatic conditions the repertoire of iNKT cells is modulated by tissue-specific signals that control iNKT cell activation and proliferation resulting in differential clonal expansion found for cells resident in various organs. Moreover, the iNKT cell TCR repertoire changes in response to lipid immunization and is shaped by age and by environmental changes. Thus, post-thymic modification of the iNKT cell TCR repertoire underpins the distinct antigen specificity of iNKT cells residing in peripheral tissues

2019-12-17 | GSE131420 | GEO

UTX controls lineage-specific epigenetic program of iNKT cells

Project description:NKT cells are innate-like lymphocytes that protect against infection, autoimmune disease, and cancer. However, little is known about epigenetic regulation of iNKT cell development. Here, we show that the H3K27me3 histone demethylase UTX is an essential cell-intrinsic factor that controls an iNKT lineage specific gene expression program and epigenetic landscape in a demethylase activity dependent manner. UTX-deficient iNKT cells exhibit impaired expression of iNKT signature genes due to a decrease in activation-associated H3K4me3 and an increase in repressive H3K27me3 marks within the promoters that UTX occupies. Notably, we identified JunB as a novel regulator of iNKT development that partners with UTX to establish an iNKT lineage specific gene expression program. Moreover, we demonstrate that UTX-mediated regulation of super-enhancer accessibility is a key mechanism for iNKT lineage commitment. These findings uncover how UTX regulates iNKT cell development through multiple epigenetic mechanisms.

2016-07-12 | GSE84238 | GEO

Gene expression profiling of WT or Dicer KO iNKT cells and T cells

Project description:iNKT cells are a T lymphocyte subset displaying an innate effector phenotype that is acquired through a thymic developmental program controlled by microRNAs (miRNAs). iNKT cells lacking all miRNAs by the deletion of Dicer (Dicer KO) are markedly reduced and display a complete maturation block. In this study, we sought to gain insight into the miRNA-regulated genetic program required for iNKT cell development. By systemic analysis, we identified transcripts differentially expressed between thymic WT or Dicer KO iNKT cells and targeted by the iNKT cell-specific miRNAs. TGF-βRII, a molecule critically implicated in iNKT cell maturation, was found upregulated in Dicer KO iNKT cells together with increased TGF-β-dependent signaling. miRNAs belonging to the paralog miR-106a~363, miR-106b~25 and miR-17~92 clusters were predicted to target TGF-βRII mRNA during iNKT cell development. Thymic iNKT cells lacking all three miRNA clusters displayed both increased TGF-βRII expression and signaling and a maturation block, recapitulating those found in Dicer KO iNKT cells. Consistently, inhibition of TGF-β-dependent signaling in the absence of miRNAs, by crossing TGF-βRII KO and Dicer KO mice, rescued iNKT cell maturation. Collectively, our results highlight a fundamental requirement of the modulation of TGF-β-dependent signaling by miRNAs for iNKT cell development

2016-11-17 | GSE79901 | GEO

iNKT gene profiling_Map3k1

Project description:Transcriptional profiling of iNKT gene expression in Map3k1 control and mutant mice

2016-06-01 | E-MTAB-1561 | biostudies-arrayexpress