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STAT3 regulates CD8+ T cell differentiation and functions in cancer [ATAC-seq]

ABSTRACT: STAT3 regulates CD8+ T cell differentiation and functions in cancer [ATAC-seq]

PROVIDER: PRJNA898636 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22200005_1.fastq.gz	Fastqsanger.gz
	SRR22200005_2.fastq.gz	Fastqsanger.gz
	SRR22200006_1.fastq.gz	Fastqsanger.gz
	SRR22200006_2.fastq.gz	Fastqsanger.gz
	SRR22200007_1.fastq.gz	Fastqsanger.gz

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STAT3 regulates CD8+ T cell differentiation and functions in cancer [ATAC-seq]

Project description:In cancer, persistent antigens drive CD8+ T cell differentiation into exhausted progenitor (Texprog) and terminally exhausted (Texterm) cells. However, how the extrinsic and intrinsic regulatory mechanisms cooperate during this process still remain not well understood. Here, we found STAT3 signaling plays essential roles in promoting intra-tumor Texterm cell development, by enhancing their effector functions and survival, which results in better tumor control. In tumor microenvironments, STAT3 is predominantly activated by IL-10 and IL-21, but not IL-6. Besides, STAT3 also plays critical roles in the development and function of terminally differentiated effector CD8+ T cells in acute infection. Mechanistically, STAT3 transcriptionally promotes the expression of effector function-related genes, while suppresses those expressed by progenitor Tex subset. Moreover, STAT3 functions in collaboration with BATF and IRF4 to mediate chromatin activation at effector gene loci. Thus, we have elucidated the roles of STAT3 signaling in terminally differentiated CD8+ T cell development, especially in cancer, which benefits developing more effective immunotherapies against tumor.

2022-12-25 | GSE217372 | GEO

STAT3 regulates CD8+ T cell differentiation and functions in cancer [RNA-seq]

2022-12-25 | GSE217375 | GEO

STAT3 regulates CD8+ T cell differentiation and functions in cancer [ChIP-seq]

2022-12-25 | GSE217374 | GEO

STAT3 regulates CD8+ T cell differentiation and functions in cancer

Project description:STAT3 regulates CD8+ T cell differentiation and functions in cancer

| PRJNA898640 | ENA

STAT3 regulates CD8+ T cell differentiation and functions in cancer [ChIP-seq]

Project description:STAT3 regulates CD8+ T cell differentiation and functions in cancer [ChIP-seq]

| PRJNA898637 | ENA

STAT3 regulates CD8+ T cell differentiation and functions in cancer [RNA-seq]

Project description:STAT3 regulates CD8+ T cell differentiation and functions in cancer [RNA-seq]

| PRJNA898641 | ENA

STAT3 regulates CD8+ T cell differentiation and functions in cancer and acute infection.

Project description:In cancer, persistent antigens drive CD8+ T cell differentiation into exhausted progenitor (Texprog) and terminally exhausted (Texterm) cells. However, how the extrinsic and intrinsic regulatory mechanisms cooperate during this process still remains not well understood. Here, we found that STAT3 signaling plays essential roles in promoting intratumor Texterm cell development by enhancing their effector functions and survival, which results in better tumor control. In tumor microenvironments, STAT3 is predominantly activated by IL-10 and IL-21, but not IL-6. Besides, STAT3 also plays critical roles in the development and function of terminally differentiated effector CD8+ T cells in acute infection. Mechanistically, STAT3 transcriptionally promotes the expression of effector function-related genes, while it suppresses those expressed by the progenitor Tex subset. Moreover, STAT3 functions in collaboration with BATF and IRF4 to mediate chromatin activation at the effector gene loci. Thus, we have elucidated the roles of STAT3 signaling in terminally differentiated CD8+ T cell development, especially in cancer, which benefits the development of more effective immunotherapies against tumors.

| S-EPMC9884582 | biostudies-literature

Effect of STAT3-/+ secretome in CD8+ T cells in vitro culture

Project description:To investigate the effect of the addition of STAT3-/+ astrocyte derived-conditioned medium in CD8+ T cells previously activated in vitro We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 CD8+ T cells cultures of STAT3- conditon and 3 CD8+ T cells cultures of STAT3+ conditon

2024-08-30 | GSE228364 | GEO

The ATAC and SAGA coactivator complexes assemble co-translationally, but their cellular localization properties and functions are distinct

Project description:To understand the precise mechanism that guide the formation of multisubunit complexes is of key importance. Nascent proteins can find and bind their interaction partners during their translation, leading to co-translational assembly. Here we demonstrate that the distinct modules of ATAC (ADA Two A Containing) and SAGA (SPT ADA GCN5 Acetyltransferase), two lysine acetyl transferase-containing transcription coactivator complexes, assemble co-translationally in the cytoplasm of mammalian cells. Fully assembled SAGA complex forms in the cytoplasm of mammalian cells and cytoplasmic SAGA acetylates non-histones proteins, before imported in the nucleus. In contrast, ATAC has no cytoplasmic functions as it cannot be detected in the cytoplasm of mammalian cells. However, fully assembled endogenous ATAC complex containing two functional modules forms and functions in the nucleus. Thus, the two related co-activators, ATAC and SAGA, assemble by using co-translational pathways, but their subcellular localization, cytoplasmic detectability and functions are distinct.

2023-09-27 | PXD038695 | Pride

Gene expression profiling of WT and STAT3-/- Tc17 CD8+ T cells

Project description:CD8+ T cells are pre-programmed for cytotoxic differentiation. However, a subset of effector CD8+ T cells (‘Tc17’) produce IL-17 and fail to express cytotoxic genes. Here, we show that the transcription factors directing IL-17 production inhibit cytotoxicity despite persistent Runx3 expression. Cytotoxic gene repression did not require the transcription factor Thpok. We further show that STAT3 restrained cytotoxic gene expression in CD8+ T cells and that RORgt represses cytotoxic genes by inhibiting the functions but not the expression of the ‘cytotoxic’ transcription factors T-bet and Eomesodermin. Thus, the transcriptional circuitry directing IL-17 expression inhibits cytotoxic functions.

2017-11-27 | GSE104144 | GEO

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