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

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

PROVIDER: PRJNA744051 | 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
	SRR15048145_1.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 [Cut&Tag]

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

| PRJNA744056 | 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

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

Brd4 Regulates the Homeostasis of CD8<sup>+</sup> T-Lymphocytes and Their Proliferation in Response to Antigen Stimulation.

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 and terminal differentiation by decreasing glycolysis. Importantly, as JQ1, a pan-BRD inhibitor, 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.

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

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Exhausted T cells recovered from chronic antigen stimulation

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Extracellular Domains of CAR Reprogram T Cell Metabolism Without Antigen Stimulation

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2023-12-11 | MSV000093637 | MassIVE

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, PBMCs from 19 recipients before and after vaccination with EV71 vaccine were collected. 14 samples pre-vaccination and 16 samples post-vaccination were detected by microarray and their gene expression signatures after stimulation with EV71 antigen were compared.

2015-09-03 | GSE72618 | GEO

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