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Multi-scale epigenomic priming of inflammatory genes enables rapid recall in human memory T helper cells

ABSTRACT: Multi-scale epigenomic priming of inflammatory genes enables rapid recall in human memory T helper cells

PROVIDER: PRJNA870082 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20047800_1.fastq.gz	Fastqsanger.gz
	SRR20047800_2.fastq.gz	Fastqsanger.gz
	SRR20047801_1.fastq.gz	Fastqsanger.gz
	SRR20047801_2.fastq.gz	Fastqsanger.gz
	SRR20047802_1.fastq.gz	Fastqsanger.gz

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Multi-scale epigenomic priming of inflammatory genes enables rapid recall in human memory T helper cells [ChIP-seq]

Project description:Memory T cells provide long-lasting defense responses through their ability to rapidly reactivate. How memory T cells efficiently ‘recall’ an inflammatory transcriptional program remains unclear. Here, we show that primary human CD4+ memory T helper (Th) cells carry three distinct activation-inducible recall gene modules that drive metabolic adaptation, T cell activation and inflammatory cytokine production. Enhancer elements controlling recall genes were epigenetically primed through the local maintenance of transcription-permissive chromatin in resting memory Th cells. At the three-dimensional level, recall genes clustered in transcriptionally permissive subnuclear compartments and resided in topologically associating domains (‘memory TADs’), in which activation-associated promoter-enhancer interactions were pre-formed. This primed epigenomic landscape was exploited by AP-1 transcription factors - including MAF - to promote rapid transcriptional activation. Finally, recall genes and their enhancers were linked to memory Th cell dysfunction in chronic inflammatory disease. Together, our results implicate multi-scale epigenomic priming - comprising a specialized three-dimensional chromatin organization - as a key mechanism underlying immunological memory.

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Project description:Multi-scale epigenomic priming of inflammatory genes enables rapid recall in human memory T helper cells [RNA-seq]

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Multi-scale epigenomic priming of inflammatory genes enables rapid recall in human memory T helper cells [ChIP-seq]

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Multidimensional epigenomic priming of inflammatory genes enables rapid recall in human memory T cells

Project description:During T cell responses, a fraction of activated cells adopts a memory phenotype and returns to quiescence. These long-lived memory T cells retain an irreversible molecular imprint that enables them to mount a secondary recall response to the same antigen that is faster and greater in magnitude than the primary response of a naive cell. Memory T cells provide long-lasting immunological protection, forming the foundation for vaccination strategies and representing prime targets for immunotherapies to treat diseases characterized by dysfunctional memory T cells - including cancer and chronic inflammation. The molecular circuitry that endows memory T cells with their rapid recall ability remains incompletely understood. Here, we applied a multi-layered 1D-3D epigenomics approach to systematically dissect the molecular program driving rapid recall in primary human Th2 cells.

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Multidimensional epigenomic priming of inflammatory genes enables rapid recall in human memory T cells

Project description:Multidimensional epigenomic priming of inflammatory genes enables rapid recall in human memory T cells

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Multi-scale epigenomic priming of inflammatory genes enables rapid recall in human memory T helper cells

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

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Priming

Project description:Priming

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Learning-Associated Astrocyte Ensembles Regulate Memory Recall

Project description:The physical manifestations of memory formation and recall are fundamental questions that remain unresolved. At the cellular level, ensembles of neurons called engrams are activated by learning events and control memory recall. Astrocytes are in close proximity to neurons and engage in a range of activities that support neurotransmission and circuit plasticity. Moreover, astrocytes exhibit experience dependent plasticity; however whether specific ensembles of astrocytes participate in memory recall remains obscure. Here we show that learning events induce c-Fos expression in a subset of hippocampal astrocytes, which subsequently regulates hippocampal circuit function. Intersectional, c-Fos based labeling of these astrocyte ensembles after learning events reveals that they are closely affiliated with engram neurons, while re-activation of these astrocyte ensembles stimulates memory recall. At the molecular level, these astrocyte ensembles exhibit elevated expression of NFIA and its selective deletion from this population suppresses memory recall. Together, our studies identify learning-associated astrocyte ensembles as a new form of plasticity that is sufficient to provoke memory recall, while implicating astrocytes as a reservoir for the storage of memories.

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