Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211389 | GEO | 2023/07/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

2023-08-08 | GSE210958 | GEO

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

2023-08-08 | GSE211023 | GEO

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

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

| PRJNA870082 | ENA

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.

2023-07-24 | GSE207738 | GEO

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

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

| PRJNA868378 | ENA

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

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

| PRJNA868704 | ENA

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

| PRJNA856988 | ENA

Establishment, maintenance, and recall of inflammatory memory.

Project description:Known for nearly a century but through mechanisms that remain elusive, cells retain a memory of inflammation that equips them to react quickly and broadly to diverse secondary stimuli. Using murine epidermal stem cells as a model, we elucidate how cells establish, maintain, and recall inflammatory memory. Specifically, we landscape and functionally interrogate temporal, dynamic changes to chromatin accessibility, histone modifications, and transcription factor binding that occur during inflammation, post-resolution, and in memory recall following injury. We unearth an essential, unifying role for the general stress-responsive transcription factor FOS, which partners with JUN and cooperates with stimulus-specific STAT3 to establish memory; JUN then remains with other homeostatic factors on memory domains, facilitating rapid FOS re-recruitment and gene re-activation upon diverse secondary challenges. Extending our findings, we offer a comprehensive, potentially universal mechanism behind inflammatory memory and less discriminate recall phenomena with profound implications for tissue fitness in health and disease.

| S-EPMC8500942 | biostudies-literature

Rapid nucleus-scale reorganization of chromatin in neurons enables transcriptional adaptation for memory consolidation.

Project description:The interphase nucleus is functionally organized in active and repressed territories defining the transcriptional status of the cell. However, it remains poorly understood how the nuclear architecture of neurons adapts in response to behaviorally relevant stimuli that trigger fast alterations in gene expression patterns. Imaging of fluorescently tagged nucleosomes revealed that pharmacological manipulation of neuronal activity in vitro and auditory cued fear conditioning in vivo induce nucleus-scale restructuring of chromatin within minutes. Furthermore, the acquisition of auditory fear memory is impaired after infusion of a drug into auditory cortex which blocks chromatin reorganization in vitro. We propose that active chromatin movements at the nucleus scale act together with local gene-specific modifications to enable transcriptional adaptations at fast time scales. Introducing a transgenic mouse line for photolabeling of histones, we extend the realm of systems available for imaging of chromatin dynamics to living animals.

| S-EPMC8099114 | biostudies-literature

Establishment, Maintenance and Recall of Inflammatory Memory

Project description:Known for nearly a century, but through mechanisms that remain elusive, cells retain a memory of inflammation that equips them to react quickly and broadly to diverse secondary stimuli. Using mouse epidermal stem cells as a model, we elucidate how cells establish, maintain and recall inflammatory memory. Specifically, we landscape and functionally interrogate temporal, dynamic changes to chromatin accessibility, histone modifications and transcription factor binding that occur during inflammation, post-resolution and in memory recall following injury. We unearth an essential, unifying role for the general stress-responsive transcription factor FOS, which partners with JUN and cooperates with stimulus-specific STAT3 to establish memory; JUN then remains with other homeostatic factors on memory domains, facilitating rapid FOS re-recruitment and gene re-activation upon diverse secondary challenges. Extending our findings, we offer a comprehensive, potentially universal mechanism behind inflammatory memory and less discriminate recall, phenomena with profound implications for tissue fitness in health and disease.

2021-07-27 | GSE171596 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data