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Activated-memory T cells influence naïve T cell fate: A non-cytotoxic function of human CD8 T cells

ABSTRACT: Activated-memory T cells influence naïve T cell fate: A non-cytotoxic function of human CD8 T cells

PROVIDER: PRJNA836546 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19145537_1.fastq.gz	Fastqsanger.gz
	SRR19145537_2.fastq.gz	Fastqsanger.gz
	SRR19145538_1.fastq.gz	Fastqsanger.gz
	SRR19145538_2.fastq.gz	Fastqsanger.gz
	SRR19145539_1.fastq.gz	Fastqsanger.gz

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Activated-memory T cells influence naïve T cell fate: A non-cytotoxic function of human CD8 T cells

Project description:T cells are endowed with the capacity to sense their environment including other T cells 48 around them. They do so to set their numbers and activation thresholds. This form of regulation has been well-studied within a given T cell population – i.e., within the naïve or memory pool; however, less is known about the cross-talk between T cell subsets. Here, we tested whether memory T cells interact with and influence surrounding naïve T cells. We report that human naïve CD8 T cells (TN) undergo phenotypic and transcriptional changes in the presence of autologous activated-memory CD8 T cells (TMem). Following in vitro co-culture with activated central memory cells (TCM), ~3% of the TN acquired activation/memory canonical markers (CD45RO and CD95) in an MHC-I dependent-fashion. Using scRNA-seq, we also observed that ~3% of the TN acquired an activated/memory signature, while ~84% developed a unique activated transcriptional profile hybrid between naïve and activated memory. Pseudotime trajectory analysis provided further evidence that TN with an activated/memory or hybrid phenotype were derived from TN. Our data reveal a non-cytotoxic function of TMem with potential to activate autologous TN into the activated/memory pool. These findings may have implications for host-protection and autoimmunity that arises after vaccination, infection or transplantation

2022-06-29 | GSE202548 | GEO

Id2-deficient NK cells acquire a naïve-like fate

Project description:Id2-deficient NK cells acquire a naïve-like fate

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Phosphatidylinositol-3-kinase p110 delta differentially restrains and directs naïve versus effector CD8+ T cell transcriptional programs Phosphatidylinositol-3-kinase p110 delta differentially restrains and directs naïve versus effector CD8+ T cell transcriptional programs

Project description:Phosphatidylinositol-3-kinase p110 delta (PI3Kp110δ) is pivotal for CD8+ T cell immune responses. To inform how PI3Kp110δ regulates CD8+ T cells, the current study focuses on PI3Kp110δ controlled transcriptional programs and reveals how PI3Kp110δ selectively induces and represses expression of key genes that create a cytotoxic T cell (CTL). The data identify differences in PI3Kp110δ regulated transcriptional programs between naïve and cytotoxic T cells including differential control of cytolytic effector molecules, costimulatory receptors and the critical inhibitory receptors CTLA4 and SLAMF6. However, common to both naïve and effector cells is PI3Kp110δ control of the production of chemokines and cytokines that orchestrate communication between the adaptive and innate immune system. The study provides a comprehensive resource for understanding how PI3Kp110δ uses multiple mechanisms dependent on Protein Kinase B/AKT, FOXO1 dependent and independent mechanisms and mitogen-activated protein kinases (MAPK) to direct CD8+ T cell fate.

2021-06-14 | PXD025046 | Pride

Phosphatidylinositol-3-kinase p110 delta differentially restrains and directs naïve versus effector CD8+ T cell transcriptional programs

2021-06-14 | PXD025061 | Pride

Id2-deficient NK cells acquire a naïve-like fate (Affymetrix data set)

Project description:All innate lymphoid cells (ILC) constitutively express and require the small helix-loop-helix protein ID2 but the functions of ID2 are not well understood in these cells. Here we show that natural killer (NK) cells, the prototypic ILC, can develop in the absence of ID2 but lose their innate properties and remain as CD27+CD11b- cells that fail to mature into cytotoxic effectors. We show that ID2 broadly limited chromatin accessibility at E protein binding sites near T lymphocyte-associated genes including multiple chemokine receptors, cytokine receptors, and signaling molecules. Moreover, ID2 prevented the conversion of CD27+CD11b- NK cells from a CD8 memory precursor-like chromatin accessibility state toward a naïve-like chromatin accessibility state, and altered their functional capacity. Finally, we demonstrate that increased expression of the naïve T cell-associated helix-loop-helix protein ID3 was required for development of ID2-deficient NK cells, indicating that completely unfettered E protein function is incompatible with NK cell development. These data solidify the roles of ID2 and ID3 as mediators of effector and naïve gene programs, respectively, and revealed a critical role for ID2 in promoting a chromatin state and transcriptional program in CD27+CD11b- NK cells that supports the innate properties of these cells and their ability to undergo cytotoxic effector differentiation.

2018-02-26 | GSE109456 | GEO

Id2-deficient NK cells acquire a naïve-like fate (ATAC-seq data set)

2018-02-26 | GSE109517 | GEO

Id2-deficient NK cells acquire a naïve-like fate (Affymetrix data set)

Project description:Id2-deficient NK cells acquire a naïve-like fate (Affymetrix data set)

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Id2-deficient NK cells acquire a naïve-like fate (ATAC-seq data set)

Project description:Id2-deficient NK cells acquire a naïve-like fate (ATAC-seq data set)

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RNAseq data for ex vivo Naïve CD8+ T cells and TCR activated 24hr in the presence or absence of PI3Kp110δ inhibitor

Project description:Phosphatidylinositol-3-kinase p110 delta (PI3Kp110δ) is pivotal for CD8+ T cell immune responses. To inform how PI3Kp110δ directs CD8+ T cell fate the current study focuses on PI3Kp110δ controlled transcriptional programs and reveals how PI3Kp110δ selectively induces and represses expression of key genes that create a cytotoxic T cell (CTL). The data identify differences in PI3Kp110δ regulated transcriptional programs between naïve and effector cytotoxic T cells including differential control of cytolytic effector molecules, costimulatory receptors and the critical inhibitory receptors CTLA4 and SLAMF6. However, common to both naïve and effector cells is PI3Kp110δ control of the production of chemokines and cytokines that orchestrate communication between the adaptive and innate immune system. The study provides a comprehensive resource for understanding how PI3Kp110δ uses multiple processes mediated by Protein Kinase B/AKT, FOXO1 dependent and independent mechanisms and mitogen-activated protein kinases (MAPK) to direct CD8+ T cell fate.

2021-06-16 | GSE169436 | GEO

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