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

Identifiers: SRA: SRP327093
BioProject: PRJNA744056
GEO: GSE179490
Study Type: 
Abstract: 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. Overall design: Examination of Brd4' binding sites throughout the genome in mouse naïve CD8+T cells.
Center Project: GSE179490
External Link: /pubmed:34512660

Related SRA data

2 ( 2 samples )
2 (3.3Gbp; 1.1Gb)
Additional objects:
File type count
fastq 4