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

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: GSE228885 | 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 [ATAC-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.

2023-11-26 | GSE244999 | GEO

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

2023-11-26 | GSE228886 | GEO

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.

2023-11-26 | GSE228887 | GEO

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

Project description:The goal of this study is to determine the impact of Tcf1 deficiency on recall capacity of central memory CD8+ T (Tcm) cells. We demonstrate that loss of Tcf1 shows limited impact on Tcm cells at resting state, but severely comprimises activation of glycolysis and other key regulators during recall response. Based on these findings, we propose that Tcf1 preprograms the responsiveness of Tcm cells to secondary challenges.

2021-11-10 | GSE177064 | GEO

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

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

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Thymic stromal lymphopoietin limits primary and recall CD8+ T cell anti-viral responses

Project description:Thymic stromal lymphopoietin (TSLP) is a cytokine that acts directly on CD4+ T cells and dendritic cells to promote progression of asthma, atopic dermatitis, and allergic inflammation. However, a direct role for TSLP in CD8+ T-cell primary responses remains controversial and its role in memory CD8+ T-cell responses to secondary viral infection is unknown. Here, we investigate the role of TSLP in both primary and recall responses using two different viral systems. Interestingly, TSLP limited the primary CD8+ T cell response to influenza but did not affect T cell function nor significantly alter the number of memory CD8+ T cells generated after influenza infection. However, TSLP inhibited memory CD8+ T cell responses to secondary viral infection with influenza or acute systemic LCMV infection. These data reveal a previously unappreciated role for TSLP on recall CD8+ T cell responses in response to viral infection, findings with potential translational implications.

2021-01-05 | GSE156875 | GEO

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.

2024-06-30 | GSE254016 | GEO

CD73+ CD127high long-term memory CD4 T cells are highly proliferative in response to recall antigens and are early targets in HIV-1 infection

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

2021-02-02 | GSE160805 | GEO

Active STAT5 in CD8 T cells imprints a T-Bet-dependent Tc-1 program with repressed IL-6/ TGFb1 signaling leading to enhanced anti-tumor responses

Project description:CD8 T cells (TCs) expressing active STAT5 (STAT5CA) transcription factors were found to be superior to un-manipulated counterparts in their long-term persistence, capacity to infiltrate a tumor, thrive in its microenvironment and induce its regression. STAT5CA induced sustained expression of genes controlling tissue homing, cytolytic granule composition, Tc-1-associated effector molecules (GranzymeB+/IFNg+/TNFa+/CCL3+ but IL-2-) and potential for secondary responses. Sustained expression of both T-Bet and Eomes transcription factors was correlated with STAT5 binding to their corresponding genes by ChIPSeq analyses. Additionally, STAT5CA-expressing CD8 TCs demonstrated reduced IL-6R/TGFbRII expression and dampened IL-6 and TGFb1 signaling. Altogether, concerted STAT5/T-Bet/Eomes regulation controls homing, recall responses and resistance to Tc-17 polarization in CD8 TCs. TCRP1A CD8 T lymphocytes were activated by their cognate P1A Ag. After 24h, an active form of Stat5 (STAT5CA) was introduced in activated cells. Culture was continued for another 48h to induce their differentiation in effector T cells. These activated T cells were injected in congeneic hosts and recovered 70 days later from hosts' spleen and lymph nodes: TCRP1A eTC-STAT5CA.

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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

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