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Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation [Cut&Tag]

ABSTRACT: Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation [Cut&Tag]

PROVIDER: PRJNA744056 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15048143_1.fastq.gz	Fastqsanger.gz
	SRR15048143_2.fastq.gz	Fastqsanger.gz
	SRR15048144_1.fastq.gz	Fastqsanger.gz
	SRR15048144_2.fastq.gz	Fastqsanger.gz

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Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation [Cut&Tag]

Project description:CD8+ T cells are major components of adaptive immunity and confer robust protective cellular immunity, which requires adequate T-cell numbers, targeted migration, and efficient T-cell proliferation. Altered CD8+ T-cell homeostasis and impaired proliferation result in dysfunctional immune response to infection or tumorigenesis. However, intrinsic factors controlling CD8+ T-cell homeostasis and immunity remain largely elusive. Here, we demonstrate the prominent role of Brd4 on CD8+ T cell homeostasis and immune response. By upregulating Myc and GLUT1 expression, Brd4 facilitates glucose uptake and energy production in mitochondria, subsequently supporting naïve CD8+ T-cell survival. Besides, Brd4 promotes the trafficking of naïve CD8+ T cells partially through maintaining the expression of homing receptors (CD62L and LFA-1). Furthermore, Brd4 is required for CD8+ T cell response to antigen stimulation, as Brd4 deficiency leads to a severe defect in clonal expansion by decreasing glycolysis. Importantly, as JQ1, the specific inhibitor of Brd4, severely dampens CD8+ T-cell immune response, its usage as an anti-tumor agent or latency-reversing agent for human immunodeficiency virus type I (HIV-1) should be more cautious. Collectively, our study identifies a previously-unexpected role of Brd4 in the metabolic regulation of CD8+ T cell-mediated immune surveillance and also provides a potential immunomodulation target.

2021-09-15 | GSE179490 | GEO

Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation.

Project description:Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation.

| PRJNA744051 | ENA

Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation [RNA-seq]

Project description:Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation [RNA-seq]

| PRJNA744057 | ENA

KLF5 and BRD4 Cut and Tag in WT U2OS and KLF5-/- U2OS cells

Project description:Cut and tag experiments to determine the binding sites of BRD4 and KLF5 in the presence and absence of KLF5 in U2OS cells

2024-12-09 | E-MTAB-14079 | biostudies-arrayexpress

Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation [RNA-seq]

Project description:Purpose: The goals of this study are to compare the differentially expressed genes between in wild type and Brd4-/- CD8+T cells. Methods: RNA extracted from wild type and Brd4-/- CD8+T cells was used to generate RNA-seq library，followed by sequencing. Results: In naïve CD8+T cells, Brd4 deletion casued 956 downregulated genes and 841 upregulated genes. In in vitro-activated CD8+T cells（18hr），Brd4 deletion resulted in 1182 downregulated genes and 789 upregulated genes. Importantly，we noticed that Brd4 is required for the migration- and glucose-related genes. expression Conclusions: Our study represents the first detailed analysis of transcriptomes in wild type and Brd4-/- CD8+T cells. Our results show that Brd4 deletion resulted in more downregulated genes exceeding the upregulated genes and the downregulation of many migration- and glucose-ralated genes. We conclude that Brd4-mediated gene expresssion program promotes glucose metabolism and cell migartion.

2021-09-15 | GSE179491 | GEO

Homo sapiens PBMCs: pre-vaccination (stimulation vs. no stimulation with EV71 antigen) vs. post-vaccination (stimulation vs. no stimulation with EV71 antigen)

Project description:To characterize the primary and recall responses to EV71 vaccines, PBMC from 19 recipients before and after vaccination with EV71 vaccine are collected and their gene expression signatures after stimulation with EV71 antigen were compared. Four-condition experiment,pre-vaccination PBMCs (stimulation vs. no stimulation with EV71 antigen) vs. post-vaccination PBMCs (stimulation vs. no stimulation with EV71 antigen)

2015-09-03 | E-GEOD-72618 | biostudies-arrayexpress

Targeting BRD4 Ameliorates Experimental Emphysema Via Suppressing both M1 and M2 alveolar macrophage polarization-3 [CUT&TAG]

Project description:BRD4 inhibition suppressed M2 macrophage polarization. Particularly, we deeply investigated the underlying molecular mechanism of how BRD4 epigenetically regulate M2 genes expression. And finished the cut&tag experiment using BRD4, H3K27ac, IRF4 as antibody to find out the binding sites change in M2 macrophage treated with ARV825.

2024-01-09 | GSE248961 | GEO

Exhausted T cells recovered from chronic antigen stimulation

Project description:Exhausted T cells recovered from chronic antigen stimulation

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Super enhancers orchestrate osteogenesis program through navigation and initiation effects of Brd4 on Zbtb16 [CUT&TAG]

Project description:We performed multiomic high-throughput sequencing to recapitulated the primary mechanism of mesenchymal stem cells osteogenesis. We analysed the H3K27ac ChIP-seq, BRD4 CUT&Tag and RNA-seq data before and after osteogenesis, and identified super enhancers (SEs) regulated osteogenic identity genes in MSCs.

2023-05-10 | GSE206155 | GEO

Extracellular Domains of CAR Reprogram T Cell Metabolism Without Antigen Stimulation

Project description:Phosphopeptides of CARs in 14g2a-based anti-GD2, Leu16 anti-CD20, rituximab anti-CD20, and RFR-LCDR anti-CD20 CAR-T cells without antigen stimulation

2023-12-11 | MSV000093637 | MassIVE

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