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Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity [ATAC-seq]

ABSTRACT: Compared with naïve CD8+ T cells, antigen-experienced effector and central memory CD8 T cells show extensive CTCF redistribution and 3D genome reorgainzation, which underlie the transcriptomic diversification as well as recall capacity in response to secondary challenges.

ORGANISM(S): Mus musculus

PROVIDER: GSE244999 | GEO | 2023/11/26

REPOSITORIES: GEO

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Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity [RNA-seq]

Project description:Compared with naïve CD8+ T cells, antigen-experienced effector and central memory CD8 T cells show extensive CTCF redistribution and 3D genome reorgainzation, which underlie the transcriptomic diversification as well as recall capacity in response to secondary challenges.

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Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity [CUT&RUN]

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Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity

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

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Tcf1 preprograms glycolysis mobilization in central memory CD8+ T cells in recall response

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Project description:HIV-1 infection rapidly leads to a loss of the proliferative response of memory CD4+ T lymphocytes, when cultured with recall antigens. We report here that CD73 expression defines a subset of resting memory CD4 T cells which highly express the alpha-chain of the receptor for IL-7 (CD127), but not CD38 or Ki-67 in vivo, yet are highly proliferative in response to mitogen and recall antigens, and to IL-7, in vitro. These cells also preferentially express CCR5 and produce IL-2. We reasoned that CD73+ memory CD4+ T cells decrease early in HIV-1 infection. We compared gene expression profiles of healthy subjects recovered CD4+CD73+ to CD4+CD73- T cells, and also CD8+CD73+ to CD8+CD73- T cells

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2021-07-27 | GSE171596 | GEO

SIKs regulate HDAC7 stabilization and cytokine recall in late-stage T cell effector differentiation

Project description:Understanding the mechanisms underlying the acquisition and maintenance of effector function during T cell differentiation is important to unraveling how these processes can be dysregulated in the context of disease and manipulated for therapeutic intervention. Herein, we report the identification of a novel regulator of murine T cell differentiation through the evaluation of a previously unreported activity of the kinase inhibitor, BioE-1197. Specifically, we demonstrate liver kinase B1 (LKB1) mediated activation of salt-inducible kinases (SIKs) epigenetically regulates cytokine recall potential in effector CD8+ and Th1 cells. Evaluation of this phenotype revealed SIK mediated phosphorylation dependent stabilization of histone deacetylase 7 (HDAC7) occurred during late-stage effector differentiation. HDAC7 stabilization increased nuclear HDAC7 levels which correlated with both global and cytokine loci specific reductions in the activating transcription mark, histone 3 lysine 27 acetylation (H3K27Ac). Accordingly, HDAC7 stabilization diminished transcriptional induction of cytokine upon re-stimulation. Inhibition of this pathway during differentiation produced effector T cells epigenetically poised for enhanced cytokine recall. This work identifies a novel target for enhancing effector T cell functionality.

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